The adrenal cortex produces three major classes of steroids:
glucocorticoids,
(2) mineralocorticoids, and
(3) adrenal androgens.
Consequently, normal adrenal function is important for
-modulating intermediary metabolism and immune responses through glucocorticoids;
blood pressure, vascular volume, and electrolytes through mineralocorticoids;
secondary sexual characteristics (in females) through androgens.
The adrenal axis plays an important role in the stress response by rapidly increasing cortisol levels.
Adrenal disorders include hyperfunction (Cushing's syndrome) and hypofunction (adrenal insufficiency) as well as a variety of genetic abnormalities of steroidogenesis.
To describe which are the common pathophysiological
features ofhead injury
To define the mechanisms of head injuries
Characteristic clinical and imaging findings
To define the management and outcome
Adrenal gland & Cushing's Disease - Seminar August 2015Arun Vasireddy
A condition that occurs from exposure to high cortisol levels for a long time.
Fewer than 1 million cases per year (India)
Treatable by a medical professional
Requires a medical diagnosis
Lab tests or imaging always required
Chronic: can last for years or be lifelong
The most common cause is the use of steroid drugs, but it can also occur from overproduction of cortisol by the adrenal glands.
Signs are a fatty hump between the shoulders, a rounded face and pink or purple stretch marks.
Treatment options include reducing steroid use, surgery, radiation and medication.
The adrenal cortex produces three major classes of steroids:
glucocorticoids,
(2) mineralocorticoids, and
(3) adrenal androgens.
Consequently, normal adrenal function is important for
-modulating intermediary metabolism and immune responses through glucocorticoids;
blood pressure, vascular volume, and electrolytes through mineralocorticoids;
secondary sexual characteristics (in females) through androgens.
The adrenal axis plays an important role in the stress response by rapidly increasing cortisol levels.
Adrenal disorders include hyperfunction (Cushing's syndrome) and hypofunction (adrenal insufficiency) as well as a variety of genetic abnormalities of steroidogenesis.
To describe which are the common pathophysiological
features ofhead injury
To define the mechanisms of head injuries
Characteristic clinical and imaging findings
To define the management and outcome
Adrenal gland & Cushing's Disease - Seminar August 2015Arun Vasireddy
A condition that occurs from exposure to high cortisol levels for a long time.
Fewer than 1 million cases per year (India)
Treatable by a medical professional
Requires a medical diagnosis
Lab tests or imaging always required
Chronic: can last for years or be lifelong
The most common cause is the use of steroid drugs, but it can also occur from overproduction of cortisol by the adrenal glands.
Signs are a fatty hump between the shoulders, a rounded face and pink or purple stretch marks.
Treatment options include reducing steroid use, surgery, radiation and medication.
Update on diagnosis and management of emergencies in cardiogenic shock. Gustavo Moreno
The aim of this article is to update the status of cardiogenic shock in particular detail in their diagnosis and especially in its current treatment on the stage of emergency. It was through the analysis of review articles that treat this condition as the main topic.
This topic contains definition, meaning, classification, pathophysiology, clinical menifestations, metabolic and general changes, management of obstetrical shock
Sex linked describes the sex-specific patterns of inheritance and presentation when a gene mutation is present on a sex chromosome rather than a non-sex chromosome. In humans, these are termed X-linked recessive, X-linked dominant and Y-linked.
Connexins (Cx) (TC# 1.A.24), or gap junction proteins, are structurally related transmembrane proteins that assemble to form vertebrate gap junctions. An entirely different family of proteins, the innexins, form gap junctions in invertebrates.[1] Each gap junction is composed of two hemichannels, or connexons, which consist of homo- or heterohexameric arrays of connexins, and the connexon in one plasma membrane docks end-to-end with a connexon in the membrane of a closely opposed cell. The hemichannel is made of six connexin subunits, each of which consist of four transmembrane segments. Gap junctions are essential for many physiological processes, such as the coordinated depolarization of cardiac muscle, proper embryonic development, and the conducted response in microvasculature. For this reason, mutations in connexin-encoding genes can lead to functional and developmental abnormalities.
Eicosanoids are signaling molecules made by the enzymatic or non-enzymatic oxidation of arachidonic acid or other polyunsaturated fatty acids (PUFAs) that are, similar to arachidonic acid, 20 carbon units in length. Eicosanoids are a sub-category of oxylipins, i.e. oxidized fatty acids of diverse carbon units in length, and are distinguished from other oxylipins by their overwhelming importance as cell signaling molecules. Eicosanoids function in diverse physiological systems and pathological processes such as: mounting or inhibiting inflammation, allergy, fever and other immune responses; regulating the abortion of pregnancy and normal childbirth; contributing to the perception of pain; regulating cell growth; controlling blood pressure; and modulating the regional flow of blood to tissues. In performing these roles, eicosanoids most often act as autocrine signaling agents to impact their cells of origin or as paracrine signaling agents to impact cells in the proximity of their cells of origin. Eicosanoids may also act as endocrine agents to control the function of distant cells.
Cerebral circulation is the movement of blood through a network of cerebral arteries and veins supplying the brain. The rate of cerebral blood flow in an adult human is typically 750 milliliters per minute, or about 15% of cardiac output. Arteries deliver oxygenated blood, glucose and other nutrients to the brain. Veins carry "used or spent" blood back to the heart, to remove carbon dioxide, lactic acid, and other metabolic products.[1] Because the brain would quickly suffer damage from any stoppage in blood supply, the cerebral circulatory system has safeguards including autoregulation of the blood vessels. The failure of these safeguards may result in a stroke. The volume of blood in circulation is called the cerebral blood flow. Sudden intense accelerations change the gravitational forces perceived by bodies and can severely impair cerebral circulation and normal functions to the point of becoming serious life-threatening conditions.
Ecosystem is system formed by the interaction of a community of organisms with their physical environment.
Ecosystem can be natural or artificial.
Ecosystem has both abiotic and biotic components.
Ecosystem has primary, secondary and tertiary function.
Human social systems and ecosystems are complex adaptive systems
Ergonomics is the study of people in their working environment.
Cushing's syndrome is the pool of signs and symptoms due to extended exposure to glucocorticoids such as cortisol.
Signs and symptoms may include high blood pressure, abdominal obesity but with thin arms and legs, reddish stretch marks, a round red face, a fat lump between the shoulders, weak muscles, weak bones, acne, and fragile skin that heals poorly.
Women may have more hair and irregular menstruation. Occasionally there may be changes in mood, headaches, and a chronic feeling of tiredness.
Usual onset: 20 – 50 years
According to UNESCO Constructivism is learning theory which places the learner at the center of the educational process on the understanding that the learner actively constructs knowledge rather than passively receiving it.
According to Brader - Araje and Jones (2002), Constructivism can be defined as “the idea that development of understanding requires the learner to actively engage in meaning-making”.
Electroencephalography (EEG): an electrophysiological monitoring method to re...Habtemariam Mulugeta
Electroencephalography (EEG) is an electrophysiological monitoring method to record electrical activity of the brain.
It is typically noninvasive, with the electrodes placed along the scalp, although invasive electrodes are sometimes used, as in electrocorticography.
EEG measures voltage fluctuations resulting from ionic current within the neurons of the brain.
As Hall says; “To look at and listen to self is often too difficult without the help of a significant figure (nurturer) who has learned how to hold up a mirror and sounding board to invite the behaver to look and listen to himself. If he accepts the invitation, he will explore the concerns in his acts and as he listens to his exploration through the reflection of the nurse, he may uncover in sequence his difficulties, the problem area, his problem, and eventually the threat which is dictating his out-of-control behavior.”
The musculoskeletal system consists of the muscles, tendons, bones and cartilage together with the joints
The primary function of which is to produce skeletal movements
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.
Follow us on: Pinterest
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
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
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.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
3. Objectives
At the end of the session, you will be able to:
Define Shock
Explain the sign and symptom of Shock
Differentiate the diagnostic modalities of Shock
Discuss the management of Shock 3
4. INTRODUCTION
Term “choc” – French for “push” or impact was
first published in 1743 by the physician LeDran
shock is a condition in which circulation fails to
meet the nutritional needs of cells and at the same
time fails to remove metabolic waste products.
4
ATLS - Student Course Manual (10 ed.). 2018. pp. 43–52, 135.
5. Definition
Shock is the state of insufficient blood flow to the
tissues of the body as a result of problems with the
circulatory system.1
Shock also known as Circulatory Failure/ Circulatory
Collapse/ circulatory shock / Hypovolemic Shock/
blood poisoning - septic shock.2
5
1. International Trauma Life Support for Emergency Care Providers (8 ed.)
2018. pp. 172–173.
2. Tintinalli, Judith E. (2010). p. 168.
6. Cont.
Shock is a life threatening situation due to poor tissue
perfusion with impaired cellular metabolism, manifested
in turn by serious pathophysiological abnormalities.1
Shock is a term used to describe the clinical syndrome
that develops when there is critical impairment of tissue
perfusion due to some form of acute circulatory failure.2
6
1. Bailey and love
2. Davidson’s
7. Cont.
Shock may be defined as inadequate delivery of oxygen
and nutrients to maintain normal tissue and cellular
function.1
The state in which profound and widespread reduction of
effective tissue perfusion leads first to reversible, and
then if prolonged, to irreversible cellular injury.2
71. Schwartz’s
2. Kumar and Parrillo ,1995
8. Incidence/Prevalence Rate
Shock from blood loss occurs in about 1–2% of trauma
cases.1
Up to 1/3 of people admitted to the ICU are in circulatory
shock.2
Of these, cardiogenic shock accounts for approximately
20%, hypovolemic about 20%, and septic shock about 60%
of cases.3
8
1. Cherkas, David (Nov 2011). PMID 22164397
2. Vincent JL, De Backer D (October 2013. 369 (18): 1726–34.
3. Cecconi M, et al (December 2014). 40 (12): 1795–815.
9. Etiology
Heart conditions (heart attack, heart failure)
Heavy internal or external bleeding, such as from a
serious injury or rupture of a blood vessel
Dehydration, especially when severe or related to heat
illness.
Infection (septic shock)
Severe allergic reaction (anaphylactic shock)
Spinal injuries (neurogenic shock)
Burns
Persistent vomiting or diarrhea 9
Elbers PW, Ince C (2006). 10 (4): 221.
20. Clinical Presentations
Hypotension - Systolic BP<100mmHg and
tachycardia - >100/min are the key signs of shock.
Symptoms of all types of shock include:
• Rapid, shallow breathing
• Cold, clammy skin
• Rapid, weak pulse
• Dizziness or fainting
• Weakness
20
International Trauma Life Support for Emergency Care Providers (8 ed.). 2018.
pp. 172–173
21. Cont.
Depending on the type of shock the following symptoms may
also be observed:
Eyes appear to stare
Anxiety or agitation
Seizures, Confusion or unresponsiveness
Low or no urine output (Urine Output<30ml/hour)
Bluish lips and fingernails
Sweating
Chest pain
Elevated or Reduced central venous pressure
Multi-Organ Failure
21
24. Diagnosis
Initial Assessment – ABC
Airway:
Does patient have mental status to protect airway?
GCS less than “eight” means “intubate” (E4 V5 M6)
Airway is compromised in anaphylaxis
Breathing:
If patient is conversing, A& B are fine Place patient on oxygen
Circulation:
Vitals (HR, BP)
IV, start fluids, put on continuous monitor
24
ATLS - (10 ed.). 2018. pp. 43–52, 135.
25. Cont.
In a trauma, perform ABCDE, not just ABC
Deficit or Disability
Assess for obvious neurologic deficit
Movement of all four extremities? Pupils?
Glasgow Coma Scale (V5, M6, E4)
Exposure
Loosening of clothing on trauma patients.
25
29. 29
• In management of trauma patients, understanding the
patterns of injury of the patient in shock will help
direct the evaluation and management.
• Blood loss sufficient to cause shock is generally of a
large volume (e.g. external, intrathoracic, intra-
abdominal, retroperitoneal, and long bone fractures).
Cont.
ATLS - (10 ed.). 2018. pp. 43–52, 135.
30. 30
• Diagnostic and therapeutic tube thoracotomy may be
indicated in unstable patients based on clinical findings
and clinical suspicion.
• Chest radiographs, pelvic radiography,
diagnostic ultrasound or diagnostic peritoneal
lavage.
Cont.
ATLS - (10 ed.). 2018. pp. 43–52, 135.
31. Investigation
CXR - consolidation
FBC – WCC elevated or low
CBC,
ABG - hypoxia, acidosis, raised lactate
ECG - low voltage, ST elevation, True Posterior MI
Urgent Echo - LV dysfunction
CT/MRI - to exclude constructive pericarditis
Blood and urine culture
31
ATLS - (10 ed.). 2018. pp. 43–52, 135.
32. Effect of shock
CARDIOVASCULAR
decrease of preload and afterload
Baroreceptor response
Release of catechol amines
Tachycardia and vasoconstriction.
RESPIRATORY
Metabolic acidosis
Inc. respiratory rate and excretion of carbon dioxide
Results in compensatory resp. alkalosis.
32Tintinalli, Judith E. (2010). pp. 174–175.
33. Cont.
RENAL AND ENDOCRINE
decreased urine output
stimulation of renin angiotensin and aldosterone
axis
release of vasopressin from hypothalamus
resulting vasoconstriction and increase Na+ and
water reabsorption.
33
34. Cont.
MICROVASCULAR
Activation of immune and coagulation systems
hypoxia and acidosis, activate complement and
prime neutrophils oxygen free radicles and
cytokine release damaged and endothelium fluids
leak out and edema ensues.
34Tintinalli, Judith E. (2010). pp. 174–175.
35. Cont.
CELLULAR
1. Cells switch from aerobic to anaerobic metabolism
2. Decreased ATP production
3. lactic acidosis
4. Glucose exhausts and aerobic respiration ceases
5. Na+/ K+ pump impaired
6. Lysosomes release autodigestive enzymes
7. mitochondria damage
8. cell death. 35
36. Metabolic Changes In Shock
CARBOHYDRATE METABOLISM
Compensated shock : Hyperglycemia due to
increased hepatic glycogenolysis.
Decompensated shock : Hypoglycemia due to
hepatic glycogen depletion & increased
consumption of glucose by tissue.
Anaerobic glycolysis occurs as assessed by high
blood levels of lactate & pyruvate. 36
37. Cont.
PROTEIN METABOLISM
Increased intracellular protein catabolism
Conversion of amino acids to urea.
Increased blood non-nitrogen protein.
FAT METABOLISM
Increased endogenous fat metabolism.
Rise of fatty acid level in blood.
37
Kumar, Vinay; et al. (2007). pp. 102–103
38. Cont.
WATER & ELECTROLYTE DISTURBANCES
Failure of sodium pumppotassium leaves the cell
(hyponatremia)causes cellular swelling.
Shock due to loss of plasma only (in
burns)hemoconcentration
38
Kumar, Vinay; et al. (2007). pp. 102–103
39. Cont.
METABOLIC ACIDOSIS
Hypoxia of kidney, renal function is impaired blood levels of acids
like lactate, pyruvate, phosphate & sulfate rise causing metabolic
acidosis.
MORPHOLOGIC COMPLICATIONS
Morphologic changes in shock are due to Hypoxia. resulting in
degeneration & necrosis in various organ.
Organs affected are : Brain, Heart, Lungs, Kidneys, Adrenals
and GIT. 39
40. Cont.
HYPOXIC ENCEPHALOPATHY
Compensated shock results in cerebral ischemia which
produce altered state of consciousness. However, if
blood pressure falls below 50 mmHg as in systemic
hypotension in prolonged shock & cardiac arrest, Brain
suffers from serious ischemic damage with loss of
cortical functions, coma,& vegetative state.
40
41. Cont.
HEART IN SHOCK
Two types of morphologic changes in Heart
1. Hemorrhage's & Necrosis: Located in
subepicardial & subendocardial region.
2. Zonal Lesion: Opaque transverse contraction
bands in a myocyte near an intercalated disc.
41
42. Cont.
SHOCK LUNG
Lungs have Dual blood supply & generally not affected by
hypovolemic shock
But in Septic shock SHOCK LUNG seen as symptoms of
ARDS including: congestion, interstitial & alveolar edema,
interstitial lymphocytic infiltrate, alveolar hyaline membrane,
Thickening & fibrosis of alveolar septa, fibrin & platelet thrombi in
pulmonary microvasculature.
42
Kumar, Vinay; et al. (2007). pp. 102–103
43. Cont.
SHOCK KIDNEY
Irreversible renal injury Important
complication of Shock.
Renal ischemia following systemic
hypotension is considered responsible for
renal changes in Shock End result is
generally anuria & death. 43
44. Cont.
ADRENALS IN SHOCK
Adrenals show stress response in SHOCK. It includes
1. Release of aldosterone in response to hypoxic kidney.
2. Release of glucocorticoids from adrenal cortex
& catecholamine like adrenaline from adrenal
medulla.
“SEVERE SHOCK RESULTS IN ADRENAL
HAEMORRHAGES”
44
45. Cont.
HYPOXIC ENCEPHALOPATHY
Compensated shock results in cerebral ischemia which
produce altered state of consciousness. However, if
blood pressure falls below 50 mmHg as in systemic
hypotension in prolonged shock & cardiac arrest, Brain
suffers from serious ischemic damage with loss of
cortical functions, coma,& vegetative state.
45
46. Cont.
GIT
Hypo perfusion of Alimentary tract Mucosal & Mural
infarction called “HAEMORRHAGIC GASTROENTEROPATHY”
In Shock due to burns, acute stress ulcers of
stomach/duodenum “CURLING’S ULCERS”
LIVER
Hypoxia, VDM is released Vasodilatation
Others include focal necrosis, fatty change, impaired
liver function.
46
Kumar, Vinay; et al. (2007). pp. 102–103
48. ISCHEMIC REPERFUSION
SYNDROME
It is the injury that occurs once the normal circulation is restored
to the tissues
Reasons:
Acidand potassium load built up leads to myocardial
depression, vascular dilatation and hypotension.
Neutrophils are flushed back into the circulation; causes further
injury to the endothelial cells of lungs and kidneys.
Results:
Acute lung and renal injury
Multiple organ failure
Death
48
Kumar, Vinay; et al. (2007). pp. 102–103
49. Classification of SHOCK
Primary (INITIAL SHOCK)
Secondary (TRUE SHOCK)
Anaphylactic (Type I immunologic reaction)
49
Guyton, Arthur; Hall, John (2006). Textbook of Medical Physiology (11th
ed.).. pp. 278–288.
50. Cont.
Initial shock is a transient and usually benign vasovagal
attack resulting from sudden reduction of venous return to
the heart caused by neurogenic vasodilatation and
consequent peripheral pooling of the blood.
It can occur immediately following:
Trauma
Severe pain
Emotional overreaction due to:
Fear
Sorrow and surprise
Sight of blood
50
51. Cont.
Primary shock can be labeled as a severe form of
syncope because Clinically Patient develops, signs and
symptoms similar to that of syncope:
Unconsciousness
Weakness
Sinking Sensation
Pale and Clammy limbs
Weak and rapid pulse and
Low Blood Pressure
51
52. Cont.
True shock is circulatory imbalance between
oxygen supply and oxygen requirements at cellular
level; hence name CIRCULATORY SHOCK.
occurs due to hemodynamic derangements with
hypo perfusion of the cells.
52
Guyton, Arthur; Hall, John (2006). Textbook of Medical Physiology (11th
ed.).. pp. 278–288.
53. Cont.
Anaphylaxis is a serious allergic reaction that is rapid
in onset and may cause death.
It typically causes : an itchy rash, throat or tongue
swelling, SOB, vomiting, lightheadedness, and low
blood pressure.
These symptoms typically come on over minutes to
hours.
53
54. Classification Based on Etiology
HYPOVOLEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
OTHER TYPES :
TRAUMATIC
NEUROGENIC
HYPOADRENAL
54
Harsh Mohan 4th ed
55. Cont.
Due to low flow(reduced stroke volume)
hypovolemic
cardiogenic
obstructive
Due to low peripheral arteriolar resistance
(vasodilatation)
septic
anaphylactic
neurogenic
Davidson’s 21st ed 55
57. Proposed by HINSHAW and COX (1972)
1. Hypovolemic shock
2. Cardiogenic shock
3. Extra cardiac obstructive shock
4. Distributive shock
Septic shock
Anaphylactic shock
Neurogenic shock 57
58. 58
• Shock due to reduced blood volume (Hypovolemic
shock or cold shock)
Traumatic shock
Hemorrhagic shock
Surgical shock
Burn shock
Dehydration shock
Proposed by HINSHAW and COX (1972)
59. • SHOCK due to increased vascular capacity (Blood volume
normal; occurs because of inadequate blood supply to the tissues
due to increased vascular capacity):
Neurogenic shock
Anaphylactic shock
Septic shock
• SHOCK due to diseases of the Heart (cardiogenic shock)
• SHOCK due to obstruction of blood flow.
59
Proposed by HINSHAW and COX (1972)
60.
61. HYPOVOLEMIC SHOCK
61
• Occurs from inadequate circulating blood
volume
• Major effects are due to decreased cardiac
output and low intra cardiac pressure
• Severity of clinical features depends on degree
of blood volume lost
ATLS - (10 ed.). 2018. pp. 43–52, 135.
66. CLASSIFICATION OF
ACUTE BLOOD LOSS
66
Class I: blood loss up to 15% (≤1000ml) mild clinical symptoms
(compensated)
Class II: blood loss 15-30% (1000-1500ml) mild tachycardia,
tachypnea, weak peripheral pulses and anxiety (mild)
Class III: blood loss 30-40% (1500-2000ml) Hypotension,
marked tachycardia [pulse >110 to 120 bpm], and confusion
(moderate)
Class IV: blood loss >40% (>2000ml) significant depression in
systolic BP, very narrow pulse pressure (severe)
67. Class I Class II Class III Class IV
Blood loss
(mL)
Up to 750 mL 750 – 1500 mL 1500- 2000mL >2000 mL
Pulse rate
& pulse
pressure
<100 normal
or decreased
>100
decreased
>120
decreased
>140
Decreased
Blood
pressure
Normal Normal Decreased Decreased
Respiratory
rate
14 – 20 20 -30 30 - 40 > 35
Urine output
mL/hr
> 30 20 -30 5 -15 Negligible
Fluid
replacement
Crystalloid Crystalloid
& blood
Crystalloid
& blood
Crystalloid
43
72. Signs & Symptoms
72
Anxiety, restlessness, altered mental state
Hypotension
A rapid, weak, thready pulse
Cool, clammy skin
Rapid and shallow respirations
Hypothermia
Thirst and dry mouth
Distracted look in the eyes
73. Compensatory Mechanisms
73
1. Adrenergic discharge
2. Hyperventilation
3. Vasoactive hormones
Angiotensin ,Vasopressin, Epinephrine
4. Collapse
5. Re-absorption of fluid from interstitial tissue
6. Resorption of fluid from intracellular to extracellular space
7. Renal conservation of body water & electrolyte.
76. General Principles In Management
Patients should be treated in ICUs preferably
Continuous electrocardiographic monitoring
Pulse oximetry
A reduction of elevated serum lactate levels is one
good indicator of successful resuscitation and is
often used as a therapeutic goal
76
77. Medical & Surgical Management
77
OBJECTIVES
a. Increase Cardiac Output
b. Increase Tissue Perfusion
The plan of action should be based on
a. Primary problem
b. Adequate fluid replacement
c. Improving myocardial contractility
d. Correcting acid base disturbances
ATLS - (10 ed.). 2018. pp. 43–52, 135.
78. • Resuscitation
• Immediate control of bleeding: Rest, Pressure Packing,
Operative Methods
• Extracellular fluid replacement:
- Infusion of fluid is the fundamental treatment
- Crystalloids, for initial resuscitation for most forms of
hypovolemic shock.
- After the initial resuscitation, with up to several liters of
crystalloid fluid, use of colloids.
• Drugs
1. Sedatives
2. Chronotropic agents
3. Inotropic agents
78
Cont.
ATLS - (10 ed.). 2018. pp. 43–52, 135.
80. DISTRIBUTIVE SHOCK
80
• As in hypovolemic shock, there is an insufficient intravascular
volume of blood
• This form of "relative" hypovolemia is the result of dilation of
blood vessels which diminishes systemic vascular resistance
• Examples of this form of shock :
Septic shock
Anaphylactic shock
Neurogenic shock
ATLS - (10 ed.). 2018. pp. 43–52, 135.
81. TRAUMATIC SHOCK
81
• Primarily due to hypovolemia from :
Bleeding externally eg: open wounds, fractures
Bleeding internally eg: ruptured liver, spleen
• Clinical features :
Presence of peripheral & pulmonary edema.
Infusion of large amount of fluid which is adequate in
hypovolemic shock is inadequate here.
ATLS - (10 ed.). 2018. pp. 43–52, 135.
82. PATHOPHYSIOLOGY
82
Traumatic tissue activates the coagulation system
↓
Release of micro-thrombi into circulation
↓
Obstruction parts of pulmonary micro vasculature
↓
Increased pulmonary vascular resistance
↓
Increased right ventricular diastolic & right atrial pressure
↓
Humoral products of thrombi induce increase in capillary permeability
↓
Loss of plasma into interstitial tissue
↓
Depletion of Vascular volume
83. MANAGEMENT
83
1. Resuscitation
2. Local treatment of trauma & control of bleeding ,
surgical debridement of ischemic & dead tissue &
immobilization of fracture.
3. Fluid replacement with Ringers lactate, Ringers
acetate, Normal saline.
4. Anticoagulation with one intravenous dose of
10,000 units of heparin
84. CARDIOGENIC SHOCK
84
• Primary dysfunction of one ventricle or the other
• Dysfunction may be due to
> Myocardial infarction
> Chronic congestive heart failure
> Cardiac arrhythmias
> Pulmonary embolism
> Systemic arterial hypertension
85.
86. Dysfunction of right ventricle right heart unable to pump
blood in adequate amount into lungs, filling of left heart
decreases , so left ventricular out put decreases.
Dysfunction of left ventricle left ventricle unable to
maintain adequate stroke volume , left ventricular output &
systemic arterial blood pressure decreases ,there is
engorgement of the pulmonary vasculature due to normal
right ventricular output, but failure of left heart
86
Cont.
Schumann, J: et al (29 January 2018).
87. • Arises when heart is compressed from outside to
decrease cardiac output , the cause may be
*Tension pneumothorax
*Pericardial tamponade
*Diaphragmatic rupture with herniation of
the bowel into the chest.
87
Cardiogenic compressive shock:
88. CLINICAL FEATURES
88
• Skin is pale & urine out put is low.
• Pulse becomes rapid & the systemic blood pressure is
low.
• Right ventricular dysfunction, neck veins are distended
& liver is enlarged.
• Left ventricular dysfunction , there are bronchial
rales & third heart sound heard.
• Gradually, the heart also becomes enlarged.
90. MANAGEMENT
90
• Air way must be cleaned
• Initial measures include supplemental oxygen and,
when systolic blood pressure permits, administration
of i.v. nitroglycerin. Insertion of an intra-aortic
balloon pump decreases ventricular after load,
improving myocardial performance
ATLS - (10 ed.). 2018. pp. 43–52, 135.
91. Cont.
Revascularization with either angioplasty or
bypass
surgery have suggested improved survival
Vasodilators
Beta-Blockers
91
ATLS - (10 ed.). 2018. pp. 43–52, 135.
92. • Cardiogenic shock can also occur after prolonged
cardiopulmonary bypass ; the stunned myocardium may
require hrs or days to recover sufficiently to support
circulation. Treatment consists of combination of
inotropic agents
• In case of pulmonary embolus it should be treated with
large doses of heparin, intravenously
92
Cont.
93. Cont.
Pain ,if present should be controlled with
sedatives like morphine
Fulminant pulmonary edema should be
controlled with diuretics.
Drugs mainly employed are Inotrophicagents
93
94. EXTRACARDIAC
OBSTRUCTIVE SHOCK
94
• Flow of blood is obstructed, which impedes circulation
and can result in circulatory arrest
• Several conditions result in this form of shock
a. Cardiac tamponade
b. Constrictive pericarditis
c. Tension pneumothorax
d. Massive pulmonary embolism
Cotran, Ramzi S.; et al. (2005).. p. 141.
102. • Treatment of choice is pericardial drainage via
surgery
• Pulmonary embolism is usually treated with
systemic anticoagulation, but when massive
pulmonary embolism causes right ventricular failure
and shock, thrombolytic therapy should be strongly
considered 102
Management
103. NEUROGENIC SHOCK
103
• Primarily due to blockade of sympathetic nervous system
loss of arterial & venous tone with pooling of blood in the
dilated peripheral venous system.
• The heart does not fill the cardiac output falls.
• Neurogenic shock caused by:
Paraplegia
Quadriplegia.
Trauma to Spinal cord.
Spinal anesthesia.
106. CLINICAL FEATURES:
Warm skin, pink & well perfused
Heart rate is rapid
Blood pressure is low
Urine output may be normal
106
Holtz, Anders; Levi, Richard (6 July 2010). Spi).. p. 63–4.
107. Pathophysiology
107
Dilatation of the systemic vasculature
↓
Decreased systemic arterial pressure
↓
Pooling of blood in systemic venules & small veins
↓
The right heart filling & stroke volume decreases
↓
Decreased pulmonary blood volume & left heart filling
↓
Discharge of angiotensin & vasopressin though they fail to
restore the cardiac output to normal
108. MANAGEMENT
108
1. Assuming Trendelenburg position - displaces blood
from systemic venules into right heart & increases
cardiac output.
2. Administration of fluids.
3. Vasoconstrictor drugs.
Phenylephrine & Metaraminol
• Only type of shock safely treated with vasoconstrictor.
• Its prompt action saves patient from immediate damage
to important organs like brain, heart & kidney.
Holtz, Anders; Levi, Richard (6 July 2010). Spi).. p. 63–4.
109.
110. VASOVAGAL / VASOGENIC SHOCK
110
• Part of neurogenic shock
• Pathophysiology: pooling of blood due
to dilatation of peripheral vascular
system particularly in the limb muscle &
in splanchnic bed.
Holtz, Anders; Levi, Richard (6 July 2010). Spi).. p. 63–4.
111. Cont.
This causes reduced venous return to the heart leading
to low cardiac output & bradycardia, blood flow to
brain is reduced causing cerebral hypoxia &
unconsciousness.
Management: Trendelenberg position -
increases cerebral flow & consciousness is
restored
111
112. PSYCHOGENIC SHOCK
112
Part of Neurogenic shock.
Occurs following sudden fright from unexpected
bad news or at the sight of horrible accident.
Effect may vary in intensity from
temporary unconsciousness to even
sudden death.
113. SEPTIC SHOCK
113
• Most often due to gram-negative & gram-positive
septicemia.
• It occurs in cases of,
-Severe septicemia
-Cholangitis
-Peritonitis
-Meningitis etc.
• The common organisms that are concerned with septic shock are
E.coli, klebsiella, aerobactor, proteus, pseudomonas, bacteroides, etc
Singer M, et al. (February 2016). JAMA. 315 (8): 801–10.
117. GRAM POSITIVE SEPSIS AND SHOCK
117
• It is usually caused by dissemination of a potent
exotoxin liberated from gram positive bacteria without
evidence of bacteremia.
• It is usually seen in Clostridium Tetany or
Clostridium Perfringes infection.
• It is basically caused due to massive fluid losses.
• Arterial resistance falls but there is no fall in
cardiac output.
• Urine output usually remains normal.
Singer M, et al. (February 2016). JAMA. 315 (8): 801–10.
118. GRAM NEGATIVE SEPSIS AND
SHOCK
118
• The most common cause of this infection is genito-
urinary infection.
• Persons who have had operations of the genito-urinary tract
are also susceptible.
• It may also be seen in patients who have undergone
tracheostomy or those with gasterointestinal system
infections.
119. • The severity may vary from mild hypotension to
fulminating septic shock which has a poor
prognosis.
• The prognosis is more favorable when the infection
is accessible to surgical drainage.
• The clinical manifestations of septic shock may be
fulminating and rapidly fatal. It is recognized initially
by the development of chills & fever of over 100
degrees.
• Two types are clearly defined
-Early warm shock.
-Late cold shock. 119
Cont.
120. EARLY WARM SHOCK
120
• In this type there is cutaneous vasodilatation.
• Toxins increase the body temperature. To bring this
down vasculature of the skin dilates. This increases the
systemic vascular resistance.
• Arterial blood pressure falls but the cardiac
output increases, because the left ventricle has
minimal resistance to pump against.
121. Cont.
Adrenergic discharge further Increases the
cardiac output. The skin remains pink,
warm & well perfused.
The pulse is high & the blood pressure low.
There are intermittent spikes of fever with
bouts of chills.
121
122. LATE COLD SHOCK
122
• There is increased vascular resistance due to release of
toxic products.
• This leads to hypovolemia with decrease in right heart filling.
• There is decreased flow to pulmonary vasculature so the
left heart filling & the cardiac output decreases.
• The knowledge of existence of a septic focus is the only factor
that differentiates septic shock from traumatic & hypovolemic
shock.
123. 123
• The only way to reduce mortality in septic shock
is by prompt diagnosis & treatment.
• It can be divided into two groups.
Treatment of the infection.
Treatment of the shock.
Management
Singer M, et al. (February 2016). JAMA. 315 (8): 801–10.
124. • Therapy of septic shock has 3 main components
• 1st, the nidus of infection must be identified and
eliminated
• 2nd, adequate organ system perfusion and function must
be maintained, guided by cardiovascular monitoring.
76
Cont.
125. • Maintenance of blood Hb level, O2 saturation
are imp therapeutic guidelines.
• 3rd therapeutic goal is to interrupt the pathogenic
sequence leading to septic shock, achieved by
inhibiting toxic mediators such as endotoxin, TNF, and
IL-1.
76
Cont.
126. • It consists of:
Fluid replacement.
Debridement & drainage of the infection.
Administration of the antibiotics.
Mechanical ventilation.
Steroids.
Vasoactive drugs.
Specific gamma globulins to bind the endotoxins.
The antibiotic polymixin E also absorbs some of
the endotoxin. 126
Cont.
127.
128. ANAPHYLACTIC SHOCK
128
Etiology :
• The most common cause of anaphylaxis is the
administration of penicillin.
• The other causes include anesthesia, dextrans, serum
injections, stings, consumption of shell fish.
Pathophysiology:
• The antigen combines with Ig E on the mast cell &
basophils releasing large amounts of histamine and slow
releasing substances of anaphylaxis.
129. Clinical features:
• It manifests as bronchospasm, laryngeal edema,
respiratory distress, hypoxia, massive vasodilatation,
hypotension and shock.
• The mortality rate is 10%.
• In the dental office this reaction can occur during or
immediately following the administration of penicillin or
LA to a previously sensitized patient.
129
Cont.
Tintinalli, Judith E. (2010). pp. 174–175.
134. Management
134
• Immediate & aggressive management is imperative if
the patient is to survive.
Step 1: Position the patient
Place the patient in a supine position with the
legs slightly elevated.
Step 2: A-B-C
Open the airway by tilting the head. Breathing &
circulation should be established carrying BLS
as needed.
Step 3: Definitive care
As soon as a systemic allergy is suspected
emergency medical help is sought.
Tintinalli, Judith E. (2010). pp. 174–175.
135. (A) Administration of epinephrinesubcutaneously
• 0.3ml of 1:1000 for adults, 0.15 for children,0.075ml forinfants.
• With decreased perfusion the absorption of epinephrine willbe
delayed.
• In such situations it can be administered sublinguallyor
intralingually.
• If the respiratory or cardiovascular regions fail to improve within 5
minutes of administration, a 2nd dose should begiven.
• Subsequent doses can be given away 5-10 minutes as needed
provided the patient is properly monitored.
(B) Administration of oxygen
• Deliver oxygen at a flow of 5-6 liters per minute by nasal hood or
full face mask at any time during the episode.
135
Cont.
Tintinalli, Judith E. (2010). pp. 174–175.
136. (C) Monitoring of vital signs
• Monitoring the patients cardiovascular & respiratory
status continuously.
• Record blood pressure & carotid heart rate at least
every 5minutes & start closed chest compression if
cardiac arrest occurs.
(D) Additional drug therapy
• After the administration of epinephrine, the other drugs
to be administered are : Antihistamines, Corticosteroids.
• These drugs are administered only after clinical
improvement is noted & are not be given during the acute
phase as they are too slow in onset.
Cont.
139. Nursing Management of Shock
Check for a response.
Give Rescue Breaths or CPR as needed.
Lay the person flat, face-up, but do not move him or
her if you suspect a head, back, or neck injury.
Raise the person's feet about 12 inches. Use a box,
etc. If raising the legs will cause pain or further
injury, keep him or her flat. Keep the person still.
139
Sharma Asha, pp 1722- 1750
140. Cont.
Do not raise the feet or move the legs if hip or leg
bones are broken. Keep the person lying flat.
Check for signs of circulation. If absent, begin CPR.
Keep the person warm and comfortable. Loosen belt
(s) and tight clothing and cover the person with a
blanket.
140
Sharma Asha, pp 1722- 1750
141. Cont.
NPO: Even if the person complains of thirst, give
nothing by mouth. If the person wants water, moisten
the lips.
Reassure the person. Make him or her as comfortable.
Fluid and blood replacement: Open IV line on both
hands with two wide bore cannulas and start fluid
rapidly as advised.
141
Sharma Asha, pp 1722- 1750
142. Cont.
Administer oxygen via face mask.
Identify the cause and treat accordingly.
Vasoactive medications to improve cardiac
contractility, i.e. Dopamine, Dobutamine,
Noradrenaline.
142
143. Self-Care at Home
Call for help and Stay with the person until help
arrives,
check the person's airway, breathing and circulation
(the ABCs).
Administer CPR if you are trained. If the person is
breathing on his or her own, continue to check
breathing every 2 minutes until help arrives.
143
Sharon Mantik 3rd Ed pp. 740-757
144. Cont.
Do NOT move a person who has a known or suspected
spinal injury (unless they are in imminent danger of
further injury).
Have the person lie down on his or her back with the
feet elevated above the head (if raising the legs causes
pain or injury, keep the person flat) to increase blood
flow to vital organs. Do not raise the head.
144
145. Cont.
Keep the person warm and comfortable.
Loosen tight clothing and cover them with a blanket.
Do not give fluids by mouth, even if the person complains
of thirst. There is a choking risk in the event of sudden
loss of consciousness.
Give appropriate first aid for any injuries.
Direct pressure should be applied to any wounds that are
bleeding significantly. 145
147. Cont.
Mitral regurgitation
Pericarditis and cardiac tamponade
Hypovolemic shock
Papillary muscle rupture
Acute valvular dysfunction
147
Alonso DR, et al . 1973 Sep. 48 (3):588-96.
148. Prognosis
The prognosis varies with the origin of shock and its
duration.
Low volume, anaphylactic, and neurogenic shock
are readily treatable and respond well to medical
therapy.
80%-90% of young patients survive hypovolemic
shock with appropriate management.
148
149. Cont.
Cardiogenic shock associated with extensive
myocardial infraction : (mortality rate up to
75%)
Septic shock, however has a mortality rate between
30% and 80% while cardiogenic shock has a
mortality rate between 70% and 90%.
149
150. Cont.
Hypovolemic, anaphylactic and neurogenic shock
are readily treatable and respond well to medical
therapy.
Perfusion of the brain may be the greatest danger
during shock.
Therefore urgent treatment is essential for a good
prognosis
150
151. NURSING PROCESS
ASSESSMENT
1. Health Perception and Management
Subjective Data
c/c: SOB/chest pain/dizziness
etc
HPI: Mr. X is a 25yr old male
married pt, presented with sob,
weakness, fainting /2day…
Hx Past: pt has Hx of HTN Rx
in the past months….
Life style changes: sport, avoid
salt, avoid smoking…
Non/prescribed: penicillin
He has visit to hospital in the
past
Objective Data
Blood Pressure: 90/60
mmHg
Heart Rate: 120bpm
2 appointment missed by the
pt in the past Rx
151
152. 2. ACTIVITY AND EXERCISE
2.1 Mobility & Self Care
Subjective Data
Appropriate bathing,
toileting, dressing,
grooming, feeding.
Good motor activities like
sitting, standing, walking,
and , opening doors.
Good home maintenance
skill
Restriction of rigorous
physical activity
Objective Data
Good balance, coordination,
abnormal movements
Good muscle tone, strength,
bulk
Good body position
152
153. 2. ACTIVITY AND EXERCISE
2.2 Respiration functioning
Subjective Data
Smoking cigarette
Shortness of breath
Objective Data
Increased respiratory rate
Decreased SpO2
Crackles in lungs
No asymmetric expansion
Tactile fremitus present
No wheezing, rales,
crackling, rhonchus sound
153
155. 3. Nutrition & Metabolism
Subjective Data
Decreased food and fluid
intake
Nausea
Vomiting
Salty food intake restriction
Objective Data
BMI: with in normal range
No edema
No scars, stretch
marks, lesions, dilated
veins, or rashes.
No organomegaly
155
156. 4. ELIMINATION
4.1 Urinary elimination
Subjective Data
Small amount of urine
Less frequent urination
Objective Data
Normal color of urine
No bladder distension,
tenderness
156
157. 4. ELIMINATION
4.2 Bowel Elimination
Subjective Data
Recent change in bowl
movement
Normal color of stool
Hx of Bowel Surgery
Objective Data
No hemorrhoids, wart, sores
or masses
No masses or tenderness
No enlargement of prostate
157
158. 5. Sleep & Rest Pattern
Subjective Data
Normal Hour of sleep: <8hr
Nap during the day: present
Satisfaction with sleep
pattern: NO
Objective Data
Frequently yawning
Decreased attention span.
Dark circles or puffiness
around the eyes.
Continual dozing
158
159. 6. Cognition & Perception
Subjective Data
Orientation to place, person
and time: absent
Pain
Fluid imbalance
Decreased oxygen supply
Inadequate blood flow
Neurological impairment
Systemic infection
Medication toxicity
Objective Data
Shallow or rapid respiration/
SOB
Abnormal cardiovascular
function/ Hypotension
History of HTN
159
160. 7. Self- Perception & Self- Concept
Subjective Data
The pt describe him self as
good person
Pt consider his illness as his
weakness
Pt. feels good most of the
time
Objective Data
Good eye contact
Personal grooming and
appearance is good
Posture and body
movements is normal
Mood and emotions are
good
Voice and speech pattern
are normal
160
161. 8. Roles & Relationship
Subjective Data
Good financial status of the
pt family
The husband & the wife
makes the decision of the
house
Family members support
each others well
No financial problem in the
family
Objective Data
Good family interactions
No behavioural signs of
dysfunction like labile
emotions, withdrawal,
irritability, poor sleeping
and eating, inability to
concentrate, and
dependency
No indicators of physical
abuse
161
162. 9. Coping & Stress Tolerance
Subjective Data
Praying relieve pt stress
Pt talk when he is worried
Little bad effect on the pt
feeling due to illness
Objective Data
Pt has sympathetic
stimulation for sudden
stressors.
162
163. 10. SEXUALITY AND
REPRODUCTION PATTERN
Subjective Data
No STI
No change in sexuality
Objective Data
No abnormal findings in
Examination of reproductive
organs
163
164. 11. Values & Beliefs Pattern
Subjective Data
Praying, fasting are among
the Religious practices that
are important to the pt
Significance of religion to
the person is high
No Impact of illness on the
patient’s belief
Objective Data
Pt. Visit clergy
Pt. seen praying
164
165. Nursing Diagnosis
Ineffective breathing patter related to the disease
process as evidenced by change in respiratory rate
Anxiety related to the disease process as evidenced
by dizziness and light headedness
Risk of infection related to hospitalization
165
166. Nursing Plan
Goal
Return the Client breathing pattern to normal level
Remove the Client anxiety completely
Avoid the Client infection risk completely
166
167. Cont.
Expected Outcome
Client breathing pattern improved in 50% after
15min oxygenation
Client anxiety decrease by half after 10 min health
education
Client risk of infection decrease by 75% after
giving prophylactic ordered medication and CASH
167
168. Intervention
Giving ordered medication and oxygenation
Health Education And Reassurance
Performing CASH
Monitoring the client changes and treat
accordingly
168
170. Shock is a life-threatening medical condition and is a
medical emergency.
Symptoms of septic shock include fever, nausea, vomiting,
and dizziness or fainting.
There are several types of shock: septic shock caused by
bacteria, anaphylactic shock caused by hypersensitivity or
allergic reaction, cardiogenic shock from heart damage,
hypovolemic shock from blood or fluid loss, and neurogenic
shock from spinal cord trauma.
Treatment for shock depends on the cause. Tests will
determine the cause and severity. Usually IV fluids are
administered in addition to medications that raise blood
pressure. 170
Summary
171. Cont.
Septic shock is treated with antibiotics and fluids.
Anaphylactic shock is treated with diphenhydramine (Benadryl),
epinephrine (an "Epi-pen"), and steroid medications (solu-medrol).
Cardiogenic shock is treated by identifying and treating the
underlying cause.
Hypovolemic shock is treated with fluids (saline) in minor cases, and
blood transfusions in severe cases.
Neurogenic shock is the most difficult to treat as spinal cord damage
is often irreversible. Immobilization, anti-inflammatories such as
steroids and surgery are the main treatments.
Shock prevention includes learning ways to prevent heart disease,
injuries, dehydration and other causes of shock.
171
172. Reference
1) ATLS - Advanced Trauma Life Support - Student Course Manual (10 ed.). American College of Surgeons.
2018. pp. 43–52, 135. ISBN 978-78-0-9968267
2) International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018.
pp. 172–173. ISBN 978-1292-17084-8.
3) Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine
(Tintinalli)). New York: McGraw-Hill Companies. p. 168. ISBN 978-0-07-148480-0.
4) Cherkas, David (Nov 2011). "Traumatic Hemorrhagic Shock: Advances In Fluid Management“
(https://web.archive.org/web/20120118152838/http://www.ebmedicine.net/store.php?paction=showProduct
&catid=8&pid=244). Emergency Medicine Practice. 13 (11). PMID 22164397
(https://pubmed.ncbi.nlm.nih.gov/22164397). Archived from the original
(http://www.ebmedicine.net/store.php?paction=showProduct&catid=8&pid=244) on 2012-01-18.
5) Vincent JL, De Backer D (October 2013). "Circulatory shock"
(https://semanticscholar.org/paper/f8eb49085615fe6fac11777ae1f36786d161dfbe). The New England
Journal of Medicine. 369 (18): 1726–34. doi:10.1056/NEJMra1208943
(https://doi.org/10.1056%2FNEJMra1208943). PMID 24171518
(https://pubmed.ncbi.nlm.nih.gov/24171518).
6) Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, Jaeschke R, Mebazaa A, Pinsky MR,
Teboul JL, Vincent JL, Rhodes A (December 2014). "Consensus on circulatory shock and hemodynamic
monitoring. Task force of the European Society of Intensive Care Medicine"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239778). Intensive Care Medicine. 40 (12): 1795–815.
doi:10.1007/s00134-014-3525-z (https://doi.org/10.1007%2Fs00134-014-3525-z). PMC 4239778
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239778). PMID 25392034
(https://pubmed.ncbi.nlm.nih.gov/25392034).
172
173. Cont.
6) Davidson’s Principles And Practice Of Medicine – 22nd ed.
7) Schwartz’s Principles Of Surgery – 8th ed.
8) Bailey & Love’s short practice of surgery
9) "Cardiogenic shock - Symptoms and causes"
(https://www.mayoclinic.org/diseases-conditions/cardiogenic-
shock/symptoms-causes/syc-20366739). Mayo Clinic. Retrieved 22 May
2020.
10) Alonso DR, Scheidt S, Post M, Killip T. Pathophysiology of cardiogenic
shock. Quantification of myocardial necrosis, clinical, pathologic and
electrocardiographic correlations. Circulation. 1973 Sep. 48 (3):588-96.
11) Elbers PW, Ince C (2006). "Mechanisms of critical illness--classifying
microcirculatory flow abnormalities in distributive shock"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1750971).Critical Care. 10
(4): 221. doi:10.1186/cc4969 (https://doi.org/10.1186%2Fcc4969).PMC
1750971 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1750971). PMID
16879732 (https://pubmed.ncbi.nlm.nih.gov/16879732).
173
174. Cont.
11) Armstrong, D.J. (2004). Shock. In: Alexander, M.F., Fawcett, J.N., Runciman, P.J. Nursing
Schumann, J; Henrich, EC; Strobl, H; Prondzinsky, R; Weiche, S; Thiele, H; Werdan, K; Frantz,
S; Unverzagt, S (29 January 2018). "Inotropic agents and vasodilator strategies for the
treatment of cardiogenic shock or low cardiac output syndrome" (https://www.ncbi.nlm.nih.gov/p
mc/articles/PMC6491099). The Cochrane Database of Systematic Reviews. 1: CD009669.
doi:10.1002/14651858.CD009669.pub3 (https://doi.org/10.1002%2F14651858.CD009669.pub
3). PMC 6491099 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6491099). PMID 29376560
(https://pubmed.ncbi.nlm.nih.gov/29376560).
12) Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al.
(February 2016). "The Third International Consensus Definitions for Sepsis and Septic Shock
(Sepsis-3)" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4968574). JAMA. 315 (8): 801–10.
doi:10.1001/jama.2016.0287 (https://doi.org/10.1001%2Fjama.2016.0287). PMC 4968574 (http
s://www.ncbi.nlm.nih.gov/pmc/articles/PMC4968574). PMID 26903338 (https://pubmed.ncbi.nl
m.nih.gov/26903338).
13) Sharma Asha, Lewis medical surgical nursing, Elsevier publication,page no 1722-
1750
14) Sharon Mantik Lewis Medical Surgical Nursing, Mosby's year book publication3rdEdition page
no 740-757
174
175. Cont.
16) Practice. Hospital and Home. The Adult.(2nd edition): Edinburgh: Churchill Livingstone.
17) Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide
(Emergency
Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 174–175. ISBN 978-0-07-
18) Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins
Basic
Pathology (8th ed.). Saunders Elsevier. pp. 102–103 ISBN 978-1-4160-2973-1
19) Guyton, Arthur; Hall, John (2006). "Chapter 24: Circulatory Shock and Physiology of Its
Treatment". In Gruliow, Rebecca (ed.). Textbook of Medical Physiology (11th ed.).
Philadelphia,
Pennsylvania: Elsevier Inc. pp. 278–288. ISBN 978-0-7216-0240-0.
20) Holtz, Anders; Levi, Richard (6 July 2010). Spinal Cord Injury
(https://books.google.com/books?
id=ZvCqdwWwGRsC&pg=PA63). Oxford University Press. p. 63–4. ISBN 978-0-19-
970681-5.
21) Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.;
Abbas,
Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier
Saunders. p. 141. ISBN 0-7216-0187-1. 175
176. ACKNOWLEDGMENT
First I would like to express my heartfelt gratitude
to WU CMHS for giving me this chance to
enhance my knowledge and skill.
Secondly I would like to thank my instructor Mr.
Wondwossen Yimam for sharing me his deep
knowledge, experience and expertise.
Last but not least I would like to thank my family
and friends in helping me in ideas and material
during my entire work.
176
Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al.(February 2016). "The Third International Consensus Definitions for Sepsis and Septic Shock(Sepsis-3)" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4968574). JAMA. 315 (8): 801–10.doi:10.1001/jama.2016.0287 (https://doi.org/10.1001%2Fjama.2016.0287). PMC 4968574 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4968574). PMID 26903338 (https://pubmed.ncbi.nlm.nih.gov/26903338).