This document discusses sudden cardiac arrest (SCA) and sudden cardiac death (SCD). SCA refers to sudden cessation of cardiac activity that may be reversible by interventions like defibrillation, while SCD is uncorrected SCA that leads to death. SCD is defined as natural death from cardiac causes within one hour of symptoms in someone who may have unrecognized heart disease. About 500,000 cases occur annually in the US, accounting for 10-15% of natural deaths. Risk factors include prior arrhythmias, low ejection fraction, heart disease, and family history. Treatment involves cardiopulmonary resuscitation, defibrillation if needed, and treating underlying causes. Advanced cardiac life support may include int
Sudden cardiac arrest (SCA) is an event caused by a problem with the heart's "electrical" system. SCA occurs when the heart suddenly stops beating. The heart’s electrical system sends signals to the heart to beat much too fast. The heart cannot beat that fast, so the heart muscle just quivers. Blood and oxygen do not reach vital organs like the brain. Then it stops altogether. The heart needs immediate treatment from an electrical shock (defibrillation) to restart the electrical system. If SCA is not treated within 7-10 minutes, it leads to sudden cardiac death.
Sudden cardiac arrest (SCA) is an event caused by a problem with the heart's "electrical" system. SCA occurs when the heart suddenly stops beating. The heart’s electrical system sends signals to the heart to beat much too fast. The heart cannot beat that fast, so the heart muscle just quivers. Blood and oxygen do not reach vital organs like the brain. Then it stops altogether. The heart needs immediate treatment from an electrical shock (defibrillation) to restart the electrical system. If SCA is not treated within 7-10 minutes, it leads to sudden cardiac death.
Sudden cardiac arrest (SCA)&Sudden cardiac death (SCD)Abdullah Ansari
INTRODUCTION
SCD : Definition
Epidemiology
Etiology
THE INITIAL ASSESSMENT
BASIC LIFE SUPPORT
CPR Steps
SELF-ASSESSMENT FOR BLS
ADVANCED CARDIAC LIFE SUPPORT
PRINCIPLES OF EARLY DEFIBRILLATION
AUTOMATED EXTERNAL DEFIBRILLATOR
SELF-ASSESSMENT FOR ACLS
Coronary artery disease (CAD) also known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease, or ischemic heart disease (IHD), is the most common type of heart disease and cause of heart attacks. The disease is caused by plaque building up along the inner walls of the arteries of the heart, which narrows the lumen of arteries and reduces blood flow to the heart.
Advanced cardiac life support or advanced cardiovascular life support (ACLS) refers to a set of clinical interventions for the urgent treatment of cardiac arrest, stroke and other life-threatening medical emergencies, as well as the knowledge and skills to deploy those interventions.
Sudden cardiac arrest (SCA)&Sudden cardiac death (SCD)Abdullah Ansari
INTRODUCTION
SCD : Definition
Epidemiology
Etiology
THE INITIAL ASSESSMENT
BASIC LIFE SUPPORT
CPR Steps
SELF-ASSESSMENT FOR BLS
ADVANCED CARDIAC LIFE SUPPORT
PRINCIPLES OF EARLY DEFIBRILLATION
AUTOMATED EXTERNAL DEFIBRILLATOR
SELF-ASSESSMENT FOR ACLS
Coronary artery disease (CAD) also known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease, or ischemic heart disease (IHD), is the most common type of heart disease and cause of heart attacks. The disease is caused by plaque building up along the inner walls of the arteries of the heart, which narrows the lumen of arteries and reduces blood flow to the heart.
Advanced cardiac life support or advanced cardiovascular life support (ACLS) refers to a set of clinical interventions for the urgent treatment of cardiac arrest, stroke and other life-threatening medical emergencies, as well as the knowledge and skills to deploy those interventions.
Cardiac arrest, also known as cardiopulmonary arrest or circulatory arrest, is the end of normal circulation of the blood due to failure of the heart to contract effectively.
Also referred as a sudden cardiac arrest (SCA).
Cardiac arrest is a medical emergency that, in certain situations, is potentially reversible if treated early.
Unexpected cardiac arrest sometimes leads to death almost immediately; this is called sudden cardiac death (SCD).
A complete Theoretical as well as practical aspects of Cardiac defibrillation with the definition,history,defibrillator and cardiovesrsion,Equipments,pre procedural consideration,care of patient before and after defibrillation,cardiac defibrillation procedure steps with rationale,complications,documentation and legal aspects
Advanced Cardiovascular Life Support (ACLS) is the pre-eminent resuscitation course for the recognition and intervention of cardiopulmonary arrest or other cardiovascular emergencies.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
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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 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
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
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.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. INTRODUCTION
Sudden cardiac arrest (SCA) and sudden
cardiac death (SCD) refer to the sudden
cessation of cardiac activity with
hemodynamic collapse.
If an intervention (e.g., defibrillation) restores
circulation, the event is referred to as SCA. If
uncorrected, an SCA event leads to death and is
then referred to as SCD.
3. DEFINITION OF SUDDEN CARDIAC
DEATH
Sudden cardiac death is defined as “natural death due
to cardiac causes in a person who may or may not have
previously recognized heart disease but in whom the
time and mode of death are unexpected.
4. In the context of time, sudden is defined for most
clinical and epidemiologic purposes as 1 hour or less
between a change in clinical status heralding the
onset of the terminal clinical event and the cardiac
arrest itself.
To satisfy clinical, scientific, legal, and social
considerations, four temporal elements must be
considered: (1) prodromes, (2) onset of terminal
event, (3) cardiac arrest, and (4) biologic death
6. EPIDEMIOLOGY OF SCD
Approx. 5,00,000 CASES IN U.S.A PER ANNUM
Accounts for 10-15% of natural deaths and 50 % deaths
from cardiac causes.
BIMODAL AGE DISTRIBUTION with peaks between
birth and 6 months of age & after 65 yrs of age
Male preponderance
May be the first presentation of cardiovascular disease
in 25% of patients
8. Prior Episode of V.TACH
Low LVEF.
Previous Myocardial Infarction.
Coronary Artery Disease
Family History of SCD.
Cardiomyopathy
Congestive Heart Failure
Long QT Syndrome.
Right Ventricular Dysplasia.
Risk Factors of Sudden Cardiac Death (SCD)
9.
10. SUDDEN CARDIAC ARREST
Abrupt cessation of cardiac mechanical function,
which may be reversible by a prompt intervention
(e.g., defibrillation) but will lead to death in its
absence.
11. Three Basic ECG Patterns with
Cardiac Arrest
Ventricular tachyarrhythmia-- ventricular fibrillation
(VF)/sustained type of pulseless ventricular
tachycardia
Ventricular asystole or a brady-asystolic rhythm with
an extremely slow rate
Pulseless electrical activity (PEA), previously referred
to as electromechanical dissociation.
15. SUDDEN CARDIAC ARREST
The probability of achieving successful resuscitation
from cardiac arrest is related to-
Interval from onset of loss of consciousness to
institution of resuscitative efforts
The setting in which the arrest occurs
The mechanism ( VT, VF, PEA, ASYSTOLE) of CA
Clinical status of the patient before the cardiac arrest.
16. SUDDEN CARDIAC ARREST
Return of circulation and survival rates as a result of
defibrillation decreases almost linearly from first to
10th min.
17. SUDDEN CARDIAC ARREST
After 5 min, survival rates are no better than 25-30% in
out of hospital setting
Outcome in ICU and other in-hospital environments is
heavily influenced by patients preceding clinical status
18. SUDDEN CARDIAC ARREST
When the mechanism is pulseless VT, the outcome is
best
VF is the next most successful
Asystole and PEA generate dismal outcome statistics
19. Successful resuscitation following cardiac arrest requires an
integrated set of coordinated actions represented by the links in the
Chain of Survival
20. The links include the following:
Immediate recognition of cardiac arrest and
activation of the emergency response system
Early CPR with an emphasis on chest
compressions
Rapid defibrillation
Effective advanced life support
Integrated post– cardiac arrest care
21. Signs and symptoms
The most reliable sign is absence of pulse
Unconsciousness/Unresponsiveness
No respiratory movements
No blood pressure
Pupils begin dilating within 45 secs.
Seizures- may or may not occur
Death like appearance
Lips and nail beds turn blue and skin turns pale
22. INITIAL RESPONSE
As soon as a cardiac arrest is suspected , confirmed, or
even considered to be impending, calling an
emergency rescue system is the immediate priority
24. The goal of this activity is to maintain viability of the
CNS, heart and other vital organs until definitive
intervention can be achieved.
Fundamental aspects of BLS include-
Immediate recognition of SCA and activation of
emergency response system
Early CPR
Rapid defibrillation with an automated external
defibrillator (when appropriate)
25. Immediate recognition and
activation of emergency response
system
If a lone rescuer finds an unresponsive adult or
witnesses an adult who suddenly collapses, after
ensuring that the scene is safe, the rescuer should
check for a response by tapping the victim at the
shoulder and by shouting at him
The trained or untrained bystander should activate the
community emergency response system, or if in an
institution with an emergency response system call
that facility’s emergency response number
26. Unresponsiveness
If the victim also has absent or abnormal breathing(ie,
only gasping) the rescuer should assume that the
victim is in cardiac arrest
27. PULSE CHECK:
▪ Studies have shown that both lay rescuers and health
care providers (HCP) have difficulty detecting a pulse.
▪The lay rescuer should not check for a pulse
▪If the HCP doesn’t definitely feel a pulse within 10 secs
he should start chest compressions.
28. EARLY CPR
A change in the 2010 AHA guidelines for CPR is to
recommend the initiation of compressions before
rescue breaths
Change from ABC to CAB
29. RESCUER SPECIFIC CPR STRATEGIES
Untrained lay rescuer:- Hands-only (chest
compression only) CPR, with an emphasis on push
hard and push fast until an AED arrives or HCP take
over
Trained lay rescuer:- should start chest compressions
first. add rescue breaths in the ratio of 30
compressions to two breaths if able to do so
HCP:- Cycle of 30:2 until an advanced air way is
placed; then continuous chest compressions with 1
breath every 6 to 8 secs.
30. Technique : chest compressions
Place victim on a firm surface in supine position
Rescuer kneeling besides victim’s chest (out of
hospital) or standing besides bed (in hospital)
Place heel of one hand over the lower half of sternum.
Heel of the other hand should be on top of the first so
that they overlap and are parallel.
Arms should be straight and perpendicular to chest of
victim
31.
32. Technique: Rescue breaths
Open airway- Head tilt and chin lift/ Jaw thrust
Mouth to mouth
Mouth to barrier device
Mouth to nose and mouth and stoma
Ventilation with bag and mask
Ventilation with supraglottic airway- LMA, esophageal
combitube, king airway device
33. Technique: Rescue breaths
To provide mouth-to-mouth rescue breaths, open the
victim’s airway- pinch the victim’s nose- and create an
airtight mouth-to-mouth seal. Give 1 breath over 1
second, take a “regular” (not a deep) breath, and give a
second rescue breath over 1 second
Advanced airway- 1 breath every 6-8 secs
ASYNCHRONOUS with compressions
43. This next step in resuscitative sequence is designed to
achieve a stable Return of Spontaneous Circulation (
ROSC), and hemodynamic stabilization
There should not be an abrupt cessation of BLS, rather
a merging and transition from one level of activity to
the next.
44. Goals of ACLS
Revert the cardiac rhythm to one that is
hemodynamically effective-by
defibrillation/cardioversion
To optimize ventilation-through placement of an
advanced airway (i.e., intubation)
To maintain and support the restored circulation-
monitoring and use of drugs
45. Basics of ACLS
Immediately after activating emergency response,
start CPR
Attach monitor/defibrillator minimizing interruptions
in CPR
Shockable rhythm- defibrillate with recommended
shock energy and immediately resume CPR for 2 mins
(5 cycles)
49. Paddles and electrode pads: anterior-lateral position
Any doubt about the presence of a pulse chest
compressions
Rhythm can be diagnosed before CPR is initiated
52. Resume CPR while charging the defibrillator
Chest compressions should switch at every 2-minute
cycle to minimize fatigue
53. Defibrillation Strategies
Waveform and Energy
Biphasic defibrillator: manufacturer’s recommended
energy dose (120-200 J)
Unaware of the effective dose range: maximal dose
54. Defibrillation Strategies
Waveform and Energy
Second and subsequent energy levels should be at
least equivalent, and higher energy levels may be
considered if available.
Monophasic defibrillator: 360 J
Subsequent shocks at the previously successful energy
level
55. Drug Therapy in VF/Pulseless VT
Amiodarone: first-line antiarrhythmic agent
Magnesium sulfate
Torsades de pointes associated with a long QT interval
60. Drug Therapy for PEA/Asystole
Vasopressor can be given as soon as feasible
Available evidence suggests that the routine use of
atropine during PEA or asystole is unlikely to have a
therapeutic benefit .
For this reason atropine has been removed from the
cardiac arrest algorithm.
61. Treating Potentially Reversible
Causes of PEA/Asystole
PEA
reversible conditions
treated successfully if those conditions are identified and
corrected
Hypoxemia: advanced airway
severe volume loss or sepsis: administration of empirical
IV/IO crystalloid.
severe blood loss: blood transfusion
pulmonary embolism: empirical fibrinolytic therapy (Class
IIa, LOE B)
tension pneumothorax: needle decompression
62. Treating Potentially Reversible
Causes of PEA/Asystole
Asystole
end-stage rhythm that follows prolonged VF or PEA, and
for this reason the
prognosis is generally much worse
63.
64.
65. MONITORING DURING CPR
Mechanical parameteres
Rate of compression: ≥ 100/min
Depth of compression: ≥2 inches (5 cm)
Rate of ventilation: 1 breath every 6-8 s (8-10
breath/min)
67. End-Tidal CO2
If PETCO2 is <10 mm Hg, it is reasonable to consider
trying to improve CPR quality by optimizing chest
compression parameters .
If PETCO2 abruptly increases to a normal value (35-40
mm Hg), it is reasonable to consider that this is an
indicator of ROSC.
68. Coronary Perfusion Pressure and Arterial
Relaxation Pressure
Increased CPP correlates with improved 24-hour
survival rates and is associated with improved
myocardial blood flow and ROSC
If the arterial relaxation “diastolic” pressure is <20 mm
Hg, it is reasonable to consider trying to improve
quality of CPR by optimizing chest compression
parameters or giving a vasopressor or both.
69. Pulse oximetry-typically does not provide a reliable
signal because pulsatile blood flow is inadequate in
peripheral tissue beds
Routine measurement of arterial blood gases during
CPR has uncertain value
Absence of cardiac motion on echocardiogaphy during
resuscitation of patients in cardiac arrest was highly
predictive of inability to achieve ROSC
71. Epinephrine
It is reasonable to consider administering a 1 mg dose
of IV/IO epinephrine every 3-5 minutes during adult
cardiac arrest .
If IV/IO access is delayed or cannot be established,
epinephrine may be given endotracheally at a dose of
2-2.5 mg.
73. Amiodarone
An initial dose of 300 mg IV/IO can be followed by 1
dose of 150 mg IV/IO.
For recurrent or refractory VF/VT.
74. Lidocaine
Considered if amiodarone is not available
The initial dose is 1-1.5 mg/kg IV.
If VF/pulseless VT persists, additional doses of 0.5-
0.75 mg/kg IV push may be administered at 5- to 10-
minute intervals to a maximum dose of 3 mg/kg.
76. SUMMARY OF UPDATES; ACLS 2010
ABC CAB
Untrained/Lay people Hand-only CPR
CPR Depth from 1 ½ to 2 inches minimum 2 inches
Minimum pauses in CPR even if needed
77. Cont……
Professional rescuers quantitative waveform
capnography confirm intubation and CPR quality
Atropine deleted from PEA & Asystole management
To reduce time to defib. AED training should not be
limited
78. Cont……
Look, Listen and Feel removed from BLS Algorithm
Continued de-emphasis on pulse check for health care
providers and no pulse check for lay persons
79. Understanding the importance of diagnosing and
treating the underlying cause is fundamental to
management of all cardiac arrest rhythms.
82. ●Initial management is focused on establishing and
maintaining hemodynamic stability and supportive
care.
●Amiodarone or lidocaine is often used to prevent
recurrent ventricular tachyarrythmia
●Therapeutic hypothermia-confers a modest
improvement in neurological outcome
● Immediate coronary angiography with
revascularization if indicated may improve survival in
pt with ischemic etiology
83. Survivors of SCA should have a detailed CVS
evaluation including:-
ECG/ECG Monitoring/24 hr ambulatory ECG
Lab:- cardiac markers, electrolytes, drug levels for
toxicity, tox screen,
Echocardiography
Electrophysiological testing
Cardiac MRI
Genetic testing for channelopathies
84. SUDDEN CARDIAC ARREST
Causes of death during hospitalization after
successfully resuscitated CA-
Anoxic encephalopathy and infections subsequent to
prolonged respirator dependence account for 60% of
deaths
30% occur as a consequence of refractory low cardiac
output states
Recurrent arrhythmias account for only 10% of in-
hospital deaths
86. PRIMARY PREVENTION
① Identifying individuals at high risk of SCD:-
▪Combination of factors more useful
▪Most imp parameter-LVEF
▪EP testing, ambulatory ECG, SAECG, HRV, T WAVE
Alternans have been used
②Pharmacological agents-
▪Beta blockers, ACEI, Amiodarone
▪Revascularisation
▪ ICD/CRT
For gen population age 35 yrs and older,SCD risk is 0.1-0.2 % per yr and that among adolescents and adults younger than age 30 yrs is 1 per 1 lakh.
Risk for SCD increases dramatically beyond age 35 yrs.
Among pt >30 yrs of age, with advanced structural hrt ds, and markers of high risk for CA, the event rate may exceed 25% per yr.
Outcome is gud for CA occuring in the icu in the presenve of acute cardiac event or transient metabolic disturbances. But survival among [patients with far advanced cardiac or noncardiac causes is no better than in out of hosp setting
Subsequent: ซึ่งตามมา
Although anecdotally administered IO without known adverse effects, there is limited experience with amiodarone given by this route.