This document discusses the management of patients with arrhythmias. It begins by defining arrhythmias and explaining their pathophysiology and manifestations. It then describes different types of arrhythmias including supraventricular arrhythmias like atrial fibrillation, ventricular arrhythmias, and inherited arrhythmias. Risk factors, causes, clinical manifestations, diagnostic tests, and treatment options like antiarrhythmic drugs, defibrillation, and pacemakers are also outlined. The treatment section provides details on the different classes of antiarrhythmic drugs and their mechanisms of action.
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Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
MANAGEMENT OF PATIENTS WITH ARRHYTHMIAS milka.pptx
1. MANAGEMENT OF PATIENTS WITH
ARRHYTHMIAS
MILKA VAIJAN LONDHE
TEACHING FELLOW
SCHOOL OF HEALTH SCIENCES
SCHOOL OF HEALTH SCIENCES
KUBANG KERIAN
KOTA BHARU
6. • RHYTHM DISTURBANCES RESULT FROM ABNORMALITIES OF
IMPULSE FORMATION, IMPULSE CONDUCTION, OR BOTH. BRADY
ARRHYTHMIAS RESULT FROM DECREASED INTRINSIC PACEMAKER
FUNCTION OR BLOCKS IN CONDUCTION, PRINCIPALLY WITHIN THE
AV NODE OR THE HIS-PURKINJE SYSTEM.
9. ATRIAL FIBRILLATION
• ATRIAL FIBRILLATION:
• Is known as AF or afib, is an
irregular, rapid heart rate that
may cause symptoms like
heart palpitations, fatigue,
and shortness of breath. AF
occurs when the upper
chambers of the heart (atria)
beat out of rhythm.
10. ATRIAL FLUTTER
• It is a common abnormal heart rhythm that starts in the atrial
chambers of the heart. When it first occurs, it is usually associated
with a fast heart rate and is classified as a type of supraventricular
tachycardia.
• Although people with atrial flutter may not experience symptoms,
the disorder can cause stroke, heart failure and other
complications.
11. ATRIAL TACHYCARDIA
• It is a type of abnormal heart rhythm, or arrhythmia. It occurs
when the electrical signal that controls the heartbeat starts from
an unusual location in the upper chambers (atria) and rapidly
repeats, causing the atria to beat too quickly.
12. ATRIOVENTRICULAR NODAL REENTRANT
TACHYCARDIA
AV NODAL REENTRANT TACHYCARDIA (AVNRT), OR ATRIOVENTRICULAR
NODAL REENTRANT TACHYCARDIA:
• IS A TYPE OF ABNORMAL FAST HEART RHYTHM. IT IS A TYPE OF
SUPRAVENTRICULAR TACHYCARDIA (SVT), MEANING THAT IT ORIGINATES
FROM A LOCATION WITHIN THE HEART ABOVE THE BUNDLE OF HIS.
13. PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PAROXYSMAL
SVT)
• Is an episodic condition with an abrupt onset and termination. SVT
in general is any tachyarrhythmia that requires atrial and/or
atrioventricular (AV) nodal tissue for its initiation and maintenance
15. WOLF-PARKINSON-WHITE SYNDROME
CONTD….
• Wolff-Parkinson -white (WPW) syndrome is a condition in
which there is an extra electrical pathway in the heart. The
condition can lead to periods of rapid heart rate (tachycardia).
• Wpw syndrome is one of the most common causes of fast
heart rate problems in infants and children.
16. VENTRICULAR ARRHYTHMIAS
• VENTRICULAR FIBRILLATION: Ventricular fibrillation is a heart
rhythm problem that occurs when the heart beats with rapid,
erratic electrical impulses. This causes pumping chambers in the
heart (the ventricles) to quiver uselessly, instead of pumping
blood. Sometimes triggered by a heart attack, ventricular
fibrillation causes blood pressure to plummet, cutting off blood
supply to the vital organs.
17. VENTRICULAR TACHYCARDIA
VENTRICULAR TACHYCARDIA:
• Is a very fast heart rhythm that begins in the ventricles. ...
Ventricular tachycardia is a pulse of more than 100 beats per
minute with at least three irregular heartbeats in a row. It is
caused by a malfunction in the heart's electrical system.
18. PREMATURE VENTRICULAR BEATS
PREMATURE VENTRICULAR CONTRACTIONS (PVCS)
• ARE EXTRA HEARTBEATS THAT BEGIN IN ONE OF HEART'S TWO
LOWER PUMPING CHAMBERS (VENTRICLES). THESE EXTRA BEATS
DISRUPT REGULAR HEART RHYTHM, SOMETIMES CAUSING TO FEEL
A FLUTTERING OR A SKIPPED BEAT IN THE CHEST.
19. INHERITED ARRHYTHMIAS
• BRUGADA SYNDROME:
IS A CONDITION THAT CAUSES A DISRUPTION OF THE HEART'S NORMAL
RHYTHM. SPECIFICALLY
• THIS DISORDER CAN LEAD TO IRREGULAR HEARTBEATS IN THE HEART'S
LOWER CHAMBERS (VENTRICLES), WHICH IS AN ABNORMALITY CALLED
VENTRICULAR ARRHYTHMIA.
20. CATECHOLAMINERGIC POLYMORPHIC
VENTRICULAR TACHYCARDIA
CATECHOLAMINERGIC POLYMORPHIC VENTRICULAR TACHYCARDIA (CPVT)
• IS A GENETIC DISORDER THAT CAUSES AN ABNORMALLY FAST AND IRREGULAR
HEART RHYTHM IN RESPONSE TO PHYSICAL ACTIVITY OR EMOTIONAL STRESS.
... WHEN A RYR2 GENE MUTATION IS INVOLVED, THE CONDITION IS PASSED
THROUGH FAMILIES IN AN AUTOSOMAL DOMINANT FASHION.
21. LONG QT SYNDROME
LONG QT SYNDROME (LQTS) IS
• A heart rhythm condition that can potentially cause fast, chaotic heartbeats.
• These rapid heartbeats might trigger a sudden fainting spell or seizure. ...
And can have a genetic mutation that puts the person at risk of being born
with congenital long qt syndrome
22. BRADYCARDIA
HEART BLOCK
is an abnormal heart rhythm where the heart beats too slowly (bradycardia ).
• in this condition, the electrical signals that tell the heart to contract are
partially or totally blocked between the upper chambers (atria) and the lower
chambers (ventricles).
23. SICK SINUS SYNDROME
SICK SINUS SYNDROME ( SSS )
• Is a relatively uncommon heart rhythm disorder. SSS is not a
specific disease, but rather a group of signs or symptoms that
indicate the sinus node, the heart's natural pacemaker, is not
functioning properly.
24. RISK FACTORS
• Coronary artery disease, other heart problems and previous heart surgery.
• High blood pressure.
• Congenital heart disease
• Thyroid problems
• . Drugs and supplements. Certain over-the-counter cough and cold
medicines
• Diabetes.
• Obstructive sleep apnea
• Electrolyte imbalance
• Drinking too much alcohol.
• Caffeine or nicotine use
25. CAUSES
• Many things can lead to, or cause, an arrhythmia,
including:
• A heart attack that's occurring right now
• Scarring of heart tissue from a prior heart attack
• Changes to heart's structure, such as from cardiomyopathy
• Blocked arteries in the heart (coronary artery disease)
• High blood pressure
• Overactive thyroid gland (hyperthyroidism)
26. CONTD…..
• Underactive thyroid gland (hypothyroidism)
• Smoking
• Drinking too much alcohol or caffeine
• Drug abuse
• Stress
• Certain medications and supplements, including over-the-counter cold and
allergy drugs and nutritional supplements
• Diabetes
• Sleep apnea
• Genetics
27. CLINICAL MANIFESTATION
• A fluttering in the chest
• A racing heartbeat (tachycardia)
• A slow heartbeat (bradycardia)
• Chest pain
• Shortness of breath
• Dizziness
• Sweating
• Fainting (syncope) or near fainting
28. PREVENTION
• Eating a heart-healthy diet
• Increasing physical activity
• Avoiding smoking
• Keeping a healthy weight
• Limiting or avoiding caffeine and alcohol
• Reducing stress, as intense stress and anger can cause heart
rhythm problems
• Using over-the-counter medications with caution, as some cold
and cough medications contain stimulants that may trigger a
rapid heartbeat
29. DIAGNOSTIC TESTS FOR ARRHYTHMIAS
• Electrocardiogram
• Holter monitor
• Echocardiogram
• Stress test
31. ANTIARRHYTHMIC DRUGS
CLASS I a AGENTS
INTERFERE WITH THE
SODIUM (NA+)
CHANNEL.
QUINIDINE
AJMALINE
PROCAINAMIDE
DISOPYRAMIDE
MECHANISM
CLASS 1 PROLONG
THE ACTION
POTENTIAL AND HAS
INTERMEDIATE
EFFECT ON THE 0
PHASE OF
DEPOLARIZATION
MEDICAL USES
VENTRICULAR
ARRHYTHMIAS
PREVENTION OF
PAROXYSMAL RECURRENT
ATRIAL FIBRILLATION
(TRIGGERED BY VAGAL
OVERACTIVITY)
PROCAINAMIDE IN
WOLFF-PARKINSON-
WHITE SYNDROME
INCREASES QT INTERVAL
32. CLASS 1b AGENT
Na+ channel block
(fast
association/dissoci
ation)
Lidnocaine
Phenytoin
Nexiletine
Tocainide
MECHANISM
Can prolong QRS
complex in
overdose
Class 1b shorten
the action potential
of myocardial cell
and has weak effect
on intiation of
phase 0 of
depolarization
MEDICAL USES
Treatment and
prevention during
and immediately
after myocardial
infarction, though
this practice is now
discouraged given
the increased risk of
asystole
Ventricular
33. CLASS 1 C AGENT
NA+ CHANNEL
BLOCK (SLOW
ASSOCIATION/DISSO
CIATION)
ENCAINIDE
FLECAINIDE
PROPAFENONE
MORICIZINE
MECHANISM
HAS NO EFFECT
ON ACTION
POTENTIAL AND
HAS THE
STRONGEST
EFFECT ON
INITIATION PHASE
0 THE
DEPOLARIZATION
MEDICAL USES
PREVENTS PAROXYSMAL
ATRIAL FIBRILLATION
TREATS RECURRENT
TACHYARRHYTHMIAS OF
ABNORMAL
CONDUCTION SYSTEM
CONTRAINDICATED
IMMEDIATELY AFTER
MYOCARDIAL
INFARCTION
35. CLASS 3
K+ CHANNEL
BLOCKER
AMIODARONE
SOTALOL
IBUTILIDE
DOFETILIDE
DRONEDARONE
E-4031
VERNAKALANT
MECHANISM
SOTALOL IS ALSO A
BETA BLOCKER[4]
AMIODARONE HAS
CLASS III MOSTLY,
BUT ALSO I, II, & IV
ACTIVITY
MEDICAL USES
IN WOLFF-PARKINSON-WHITE
SYNDROME
(SOTALOL:) VENTRICULAR
TACHYCARDIAS AND ATRIAL
FIBRILLATION
(IBUTILIDE:) ATRIAL FLUTTER
AND ATRIAL FIBRILLATION
(AMIODARONE): PREVENTION
OF PAROXYSMAL ATRIAL
FIBRILLATION,[6] AND
HAEMODYNAMICALLY
STABLE VENTRICULAR
TACHYCARDIA
36. CLASS 4 AGENTS
CALCIUM CHANNEL
BLOCKERS
VERAPAMIL
DILTIAZEM
MECHANISM
CALCIUM
CHANNEL
BLOCKER
MEDICAL USES
PREVENT RECURRENCE
OF PAROXYSMAL
SUPRAVENTRICULAR
TACHYCARDIA
REDUCE VENTRICULAR
RATE IN PATIENTS WITH
ATRIAL FIBRILLATION
37. CLASS 5
Adenosine
Digoxin
Magnesium
sulfate
MECHANISM
Work by other or
unknown
mechanisms
(direct nodal
inhibition)
MEDICAL USES
Used in
supraventricular
arrhythmias,
especially in heart
failure with atrial
fibrillation,
contraindicated in
ventricular
arrhythmias. Or in the
case of magnesium
38. DEFIBRILLATION
• DEFIBRILLATION - Is the
treatment for immediately life-
threatening arrhythmias with
which the patient does not have
a pulse, ie ventricular fibrillation
(VF) or pulseless ventricular
tachycardia (VT).
• CARDIOVERSION - Is any
process that aims to convert an
arrhythmia back to sinus
39. • Cardioversion is a medical procedure that restores a normal heart
rhythm in people with certain types of abnormal heartbeats
(arrhythmias).
Why it's done
• Cardioversion can correct a heartbeat that's too fast (tachycardia)
or irregular (fibrillation). Cardioversion is usually used to treat
people who have atrial fibrillation or atrial flutter.
40. DEFIBRILLATION
• DEFIBRILLATION IS DONE
AT THE TIME OF
EMERGENCY
CARDIOVERSION
• CARDIOVERSION IS SAME
AS DEFIBRILLATION , BUT
IT IS PLANNED
41. COMPLICATIONS
• Dislodged blood clots: Some people who have irregular heartbeats have blood
clots in their hearts. Electric Cardioversion can cause these blood clots to
move to other parts of your body. This can cause life-threatening
complications, such as a stroke or a blood clot traveling to your lungs
(pulmonary embolism).
• Abnormal heart rhythm: In rare cases, some people who undergo
Cardioversion end up with other heart rhythm problems during or after their
procedure. This is a rare complication.
• Skin burn: Rarely, some people have minor burns on their skin where their
42. NURSING DIAGNOSIS:
• Knowledge deficit related to cardioversion ( defibrillator)
procedure evidenced by frequently questions
Objective:
• Patient verbalizes the knowledge regarding cardioversion
(defibrillation), pre, during and post care after cardioversion
Interventions:
Followed in the next slides
43. NURSING RESPONSIBILITIES BEFORE THE PROCEDURE
• Do not allow the patient to eat or drink anything for about 8 hours before
your procedure. If medications has to be taken before the procedure, allow
him to sip only enough water to swallow the pills.
• Before cardioversion, the procedure called a transesophageal
echocardiogram (TEE) is done to check for blood clots in the heart, which
can be dislodged by cardioversion, causing life-threatening complications
• In a transesophageal echocardiogram, throat is numbed and a flexible tube
containing a transducer is guided down the throat and into esophagus,
which connects the mouth to the stomach. From there, the transducer can
obtain more-detailed images of the heart so that your doctor can check for
blood clots.
44. NURSES RESPONSIBILITY DURING THE PROCEDURE
• A nurse will place several large patches called electrodes on the chest. The
electrodes will be connected to a cardioversion machine (defibrillator) using
wires.
• The defibrillator will record the heart rhythm throughout the procedure and
will deliver shocks to the heart to restore a normal heart rhythm. This
machine can also correct the heart's rhythm if it beats too slowly after
cardioversion
• Before the shocks are delivered, a nurse will insert an intravenous (IV) line in
the arm. The IV line is used to give the medications that will make patient to
sleep during the procedure so that patient won't feel any pain from the
shocks. the IV line can be used to give additional medications that can help
restore the heart rhythm.
45. NURSING RESPONSIBILITY AFTER THE
PROCEDURE
• Electric cardioversion is done on an outpatient basis, meaning
patient can go home on the same day procedure is done. Patient
will spend an hour or so in a recovery room being closely
monitored for complications.
•IN CASE OF DEFIBRILLATION ( EMERGENCY )
PATIENT WILL REMAIN IN THE HOSPITAL TILL HE
GETS RECOVERED COMPLETELY….
46. NURSES RESPONSIBILITIES ( EDUCATION TO THE
PATIENT AFTER THE PROCEDURE)
• Avoid or limit caffeine and alcohol.
• Use less salt (sodium), which can help lower blood pressure.
• Increase physical activity.
• Quit smoking.
• Eat heart-healthy foods and maintain a healthy weight.
• Try to limit or manage stress and anger.
47. PACEMAKER
• A device for stimulating the
heart muscle and regulating
its contractions.
• A pacemaker is a small
device with two parts — a
generator and wires (leads,
or electrodes) — that's
placed under the skin in the
chest to help control the
heartbeat
48. WHO NEEDS PACEMAKER
•Cardiac arrhythmias
•Aging-where heart muscle damage
•Some medications- like medicines of cough and
cold
•Genetic condition which causes the abnormal heart
49. WHY ITS DONE
• Pacemakers are implanted to help control the heartbeat. They
can be implanted temporarily to treat a slow heartbeat after a
heart attack, surgery or overdose of medication.
• Pacemakers can also be implanted permanently to correct a slow
heartbeat (bradycardia) or, in some cases, to help treat heart
failure.
• Device can be implanted directly into the heart, where it emits an
electrical impulse to control the heartbeat.
50. WHAT A PACEMAKER DOES
• An implanted electronic pacemaker mimics the action of natural
pacemaker. An implanted pacemaker consists of two parts:
• The pulse generator: This small metal container houses a battery
and the electrical circuitry that regulates the rate of electrical
pulses sent to heart.
• Leads (electrodes). One to three flexible, insulated wires are each
placed in a chamber, or chambers, of the heart and deliver the
electrical pulses to adjust the heart rate.
51. • Pacemakers monitor the heartbeat and, if it's too slow, the
pacemaker will speed up your heart rate by sending electrical
signals to the heart. In addition, most pacemakers have sensors
that detect body motion or breathing rate, which signals the
pacemaker to increase the heart rate during exercise to meet
body's increased need for blood and oxygen.
52. • NURSING DIAGNOSIS:
• Knowledge deficit regarding pacemaker evidenced by frequently
asked questions
• OBJECTIVE:
• Patient verbalizes the knowledge regarding the procedure,
complications
• INTERVENTIONS:
• Followed in the next slides
53. COMPLICATIONS
• Infection where the pacemaker was implanted
• Allergic reaction to the dye or anesthesia used during your
procedure
• Swelling, bruising or bleeding at the generator site
• Damage to the blood vessels or nerves near the pacemaker
• Collapsed lung
54. HOW TO PREPARE THE PATIENT
• Electrocardiogram
• Holter monitoring.
• Echocardiogram.
• Stress test
58. SPECIAL INSTRUCTIONS TO THE PATIENT
Cellphones: it's safe to talk on a cellphone, but avoid placing the cellphone
directly over the pacemaker implantation site when the phone is turned on.
Although unlikely, pacemaker could misinterpret the cellphone signal as a
heartbeat and withhold pacing, producing symptoms, such as sudden
fatigue.
Security systems. Passing through an airport metal detector won't interfere
with pacemaker, although the metal in it may sound the alarm. But avoid
lingering near or leaning against a metal-detection system.
59. Medical equipment:
• if a doctor is considering any medical procedure that involves intensive
exposure to electromagnetic energy, tell him or her that you have a
pacemaker. Such procedures include magnetic resonance imaging, therapeutic
radiation for cancer treatment and shock wave lithotripsy, which uses shock
waves to break up large kidney stones or gallstones.
POWER GENERATING EQUIPMENT:
• Stand at least 2 feet (60 centimeters) from welding equipment, high-voltage
transformers or motor-generator systems. If the patient work around such
equipment, doctor can arrange a test in the workplace to determine whether it
affects the pacemaker.
60. NURSING INTERVENTION FOR DYSRHYTHMIAS (
ARRHYTHMIAS)
Nursing diagnosis:
• Chest discomfort/chest pain secondary to cardiac dysrhythmias
associated with altered myocardial automaticity, conductivity or
contractibility
Objective:
Reduce chest discomfort/pain
Interventions:
Assess for signs of ineffective perfusion by system
Renal: oliguria, anuria
Gastrointestinal: nausea, hypoactive or absent bowel sounds
61. • Peripheral: Odema, altered skin colour, temperature, sensation or
integrity, weak or absent pulse
• Cerebral: dizziness, altered mental status, confusion, anxiety,
syncope, altered pupillary response, speech abnormality
• Cardiopulmonary: Hypotension, abnormal respiratory rate, capillary
refill more than 3 seconds, chest pain, dyspnea, crackles and
wheezes, jugular vein distention
• Intervention:
• Assess for and report signs/symptoms of cardiac dysrhythmias
(e.g. irregular apical pulse, adult pulse rate below 60 or above 100
beats/minute, apical-radial pulse deficit, syncope, palpitations).
62. Reduce cardiac workload
• Position patient to minimizes discomfort and facilitate respiration.
• Minimize anxiety with calm reassurance and education.
• Communicate rationale for monitoring and treatments.
• Discuss the benefits calm with the patient and family.
Initiate EKG monitor and pulse oximetry per policy.
IV access, O2, medication and 12 lead-EKG as ordered, monitor vital signs.
• Positive inotropic agents (e.g. dobutamine, dopamine) to increase myocardial
contractility
• Vasodilators (e.g. nitroglycerin) to decrease cardiac workload
• ACE inhibitors (e.g. captopril, ramipril) to decrease cardiac workload
• Diuretics for elevated capillary wedge pressure
• Morphine sulfate to reduce pain, preload and anxiety.
63. Anticipate the need to initiate cardiopulmonary resuscitation.
Assess for contributing factors: pain, fluid and electrolyte
imbalance, drug toxicity (especially digoxin), medication non-
adherence.
Provide psychosocial support for patient and family members.
• If the dysrhythmia is a life-threatening type, encourage the family
unit to calmly formulate a plan of action.
• Reassure the patient will receive the best care in keeping with his
written directives or medical power of attorney.
• Communicate the availability and value of social services as