This document discusses different types of shock and their pathophysiology. It begins with learning objectives about shock states and types of shock including cardiogenic, hypovolemic, septic, neurogenic, anaphylactic, and obstructive shock. It then covers the stages of shock and discusses specific types in more detail, focusing on their causes, pathophysiology, clinical manifestations, diagnosis, and management. The types of shock discussed in depth include hypovolemic, cardiogenic, distributive (septic, neurogenic, anaphylactic), and obstructive shock.
Disseminated intravascular coagulation (DIC) is a syndrome in which either the extrinsic or intrinsic or both pathways are activated to produce multiple fibrin clots in small blood vessels.
Thrombocytopenia is most frequently encountered Hematological problem in hospitalized patients. The most common causes and differential diagnosis of In-patient and Outpatient presentations of Thrombocytopenia is discussed here. Useful for Internal Medicine Boards . Archer Internal Medicine Board review lectures will be released soon.
It includes new definition, pathophysiology, management of sepsis, septic shock and neutropenic sepsis and even newer evolving concepts or types of sepsis.
This PPT covers pathophysiology of thrombocytopenia which includes causes of thrombocytopenia, symptoms of thrombocytopenia and diagnosis of thrombocytopenia
This topic covers the etiology, types, pathogenesis and management of Shock. It is very important for MBBS Students both theoretical & clinical aspect. Also they should know the hemodynamics across the types of shock in treating the patients....
Disseminated intravascular coagulation (DIC) is a syndrome in which either the extrinsic or intrinsic or both pathways are activated to produce multiple fibrin clots in small blood vessels.
Thrombocytopenia is most frequently encountered Hematological problem in hospitalized patients. The most common causes and differential diagnosis of In-patient and Outpatient presentations of Thrombocytopenia is discussed here. Useful for Internal Medicine Boards . Archer Internal Medicine Board review lectures will be released soon.
It includes new definition, pathophysiology, management of sepsis, septic shock and neutropenic sepsis and even newer evolving concepts or types of sepsis.
This PPT covers pathophysiology of thrombocytopenia which includes causes of thrombocytopenia, symptoms of thrombocytopenia and diagnosis of thrombocytopenia
This topic covers the etiology, types, pathogenesis and management of Shock. It is very important for MBBS Students both theoretical & clinical aspect. Also they should know the hemodynamics across the types of shock in treating the patients....
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Sepsis is the systemic inflammatory response syndrome (SIRS) due to severe infection. Sepsis simply is a Race to death between the host immune system and the pathogens. Micro-organisms grow out of control => hyperinflammatory response, With this insidious pathology the body attacks itself (auto immunity) leading to life threatening risk of organ dysfunction, septic shock and death. Micro-organisms can invade the body through wounds, IV lines, catheters etc. Sepsis kills more than 210,000 people in the US /year. It kills about 1,400 people worldwide every day. Significant decrease in Mortality due to increased Recognition and early Treatment.
shock is a Life threatening clinical syndrome of cardio-vascular collapse characterized by Hypotension and Hypoperfusion. If uncompensated, these mechanisms may lead to impaired cellular metabolism and death.
Zavras-Kounis syndrome simultaneously with reactional myoclonus post-streptok...YasserMohammedHassan1
Rationale: Drug-associated adverse effects are one of the most important entities in clinical medicine. Involuntary movements may have a dynamic serious impact on myocardial muscle. Myoclonus is well as abnormal involuntary movements with a distinct description. Myoclonus is a physical trauma and stress for coronary arteries. Physical and mechanical stress may be causing coronary artery spasm. Drug-inducing allergic angina, allergic coronary artery spasm, and allergic myocardial infarction are renowned as Zavras-Kounis syndrome. Streptokinase is a still-known effective thrombolytic in myocardial infarction. There is a correlation between COVID-19 infection and myocardial infarction. Patient concerns: A 70-year-old married, farmer, smoker, Egyptian male patient was admitted to the critical care unit with acute inferior myocardial infarction and suspected COVID-19 pneumonia. An interlacing generalized myoclonus and allergic coronary artery spasm occurred. Diagnosis: Reactional myoclonus with allergic coronary artery spasm post-streptokinase in COVID-19 inducing myocardial infarction. Interventions: Electrocardiography, oxygenation, streptokinase intravenous infusion, and echocardiography. Outcomes: Reactional generalized myoclonus with coronary artery spasm had happened during-streptokinase infusion but the dramatic response was the result. Lessons: Dramatic clinical and electrocardiographic response after using the traditional anti-allergic signifying its role and suggest the diagnosis of Zavras-Kounis syndrome. The presence of continuing generalized myoclonus movements with the disappearance of coronary artery spasm after stoppage may be directed to the myoclonus cause. Streptokinase causing generalized myoclonus movements previously unknown, so it is a new recording adverse effect finding. The presence of involuntary movements, COVID-19 pneumonia, myocardial infarction, elderly, and cigarette smoking are prognostic factors for the severity of the disease.
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.
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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
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ASA GUIDELINE
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
2. Marc Imhotep Cray, M.D.
Learning Objectives
2
1. Discuss the general concepts associated with shock states,
including physiologic response to shock, and shock
progression.
2. Describe cardiogenic shock, including pathophysiology,
clinical manifestations, diagnosis, and management.
3. Discuss hypovolemic shock, including pathophysiology,
clinical manifestations, diagnosis, and management.
4. Explain the septic type of distributive shock, including
pathophysiology, clinical manifestations, diagnosis, and
management.
By the end of this lecture the learner should be able to:
3. Marc Imhotep Cray, M.D.
Learning Objectives
3
5. Discuss the neurologic and anaphylactic types of
distributive shock, including the pathophysiology, clinical
manifestations, diagnosis, and management of each type.
6. Describe the major causes of obstructive shock, including
the pathophysiology, clinical manifestations, diagnosis, and
management of each cause
7. Discuss use of pharmacotherapy in the management of
shock states.
By the end of this lecture the learner should be able to:
4. Marc Imhotep Cray, M.D.
Shock Capsule
4
Shock is a clinical condition characterized by a fast pulse rate
(usually > 100 beats/min) and a low blood pressure (systolic
blood pressure usually < 100 mmHg)
Common types of shock are
hypovolemic (low blood volume, e.g. in hemorrhage),
cardiogenic (heart pump failure, e.g. in myocardial infarction)
septic (severe infection)
Less common types are
anaphylactic (type I hypersensitivity reaction, e.g. penicillin
allergy)
neurogenic (loss of sympathetic vasomotor tone, e.g. in a
spinal cord injury)
5. Marc Imhotep Cray, M.D.
Shock, Pathology of Different Types,
Animation_Alila Medical Media
5Online Version
6. Marc Imhotep Cray, M.D.
Stages of Shock
6
As stated above Shock is a progressive disorder that
leads to death if underlying causes are not corrected
Exact mechanisms of sepsis-related death are still unclear;
aside from increased lymphocyte and enterocyte apoptosis,
cellular necrosis is minimal
• Death typically follows the failure of multiple organs usually offer no
morphological clues to explain their dysfunction
For hypovolemic and cardiogenic shock pathways leading to a
patient’s demise are reasonably well understood tissue ischemia,
acute tubular necrosis, lactic acidosis severe cellular and tissue
injury cardiopulmonary arrest
Unless insult is massive and rapidly lethal (e.g., exsanguination
from a ruptured aortic aneurysm), shock tends to evolve through
three general (albeit somewhat artificial) stages…
7. Marc Imhotep Cray, M.D.
The 3 Stages of Shock
7
These stages have been documented most clearly in
hypovolemic shock but are common to other forms as well:
Stage 1 An initial nonprogressive stage during which reflex
compensatory mechanisms are activated and vital organ perfusion
is maintained
Stage 2 A progressive stage characterized by tissue hypoperfusion
and onset of worsening circulatory and metabolic derangement,
including acidosis
Stage 3 An irreversible stage in which cellular and tissue injury is so
severe that even if hemodynamic defects are corrected, survival is
not possible
8. Marc Imhotep Cray, M.D.
Shock, Circulatory Defined
8
Circulatory shock, commonly known as just shock, is a serious, life-
threatening medical condition where insufficient blood flow
reaches body tissues
As blood carries oxygen and nutrients around body, reduced flow
hinders delivery of these components to tissues, and can stop
tissues from functioning properly
The process of blood entering tissues is called perfusion, so when
perfusion is not occurring properly this is called a hypoperfusional
(hypo = below) state
9. Marc Imhotep Cray, M.D.
Shock (circulatory)
9
Effects of inadequate perfusion on cell function
Learn more from Dr. Najeeb’s Video Series on Circulatory shock
10. Marc Imhotep Cray, M.D.
The problem in shock
10
From: http://www.cvpharmacology.com/clinical
topics/hypotension.htm
• Altered circulatory
parameters
• Compromised
microcirculation
• Persistent severe
hypoxia
• Multiple organ failure
12. Marc Imhotep Cray, M.D.
Classification of Shock
12
• In 1972 Hinshaw and Cox suggested following
classification which is still used today
• It uses four types of shock:
1. hypovolemic
2. cardiogenic
3. distributive and
4. obstructive shock
13. Marc Imhotep Cray, M.D.
Classification
(Based on cardiovascular characteristics, which was initially proposed
in 1972 by Hinshaw and Cox.)
13
Hypovolemic
Hemorrhagic
Fluid depletion
Increased vascular capacitance
Cardiogenic
Myopathic
Mechanical
Arrhythmic
Distributive
Septic, etc.
Obstructive
PE, pericarditis, pnumothorax etc.
14. Marc Imhotep Cray, M.D.
Hypovolemic shock
14
Hypovolemic shock
This is most common type of shock and based on insufficient
circulating volume = circulating shock
• Its primary cause is loss of fluid from circulation from either an
internal or external source
• An internal source may be hemorrhage
• External causes may include extensive bleeding, high output
fistulae (greater than 500 ml per day)or severe burns
15. Marc Imhotep Cray, M.D.
Hypovolemic Shock
15
Low central venous pressure (CVP), Low pulmonary capillary wedge
pressure (PCWP), Low cardiac output (CO) and cardiac index (CI), and high
SVR arterial blood pressure may be normal or low
Loss in circulatory volume
• Decreased venous return
• Decreased filling of cardiac chambers
• Decreased cardiac output
• increase in systemic vascular resistance (SVR)
17. Marc Imhotep Cray, M.D.
Cardiogenic shock
17
Cardiogenic shock
This type of shock is caused by failure of heart to pump
effectively
• This can be due to damage to heart muscle, most often
from a large myocardial infarction
• Other causes of cardiogenic shock include
o arrhythmias,
o cardiomyopathy,
o congestive heart failure (CHF), and
o cardiac valve problems
18. Marc Imhotep Cray, M.D.
Cardiogenic Shock (2)
18
• dependent on poor pump function
• acute catastrophic failure of LV pump function
High PCWP, low CO and CI, and generally a high SVR
19. Marc Imhotep Cray, M.D.
Cardiogenic (3)
19
Myopathic
• Myocardial infarction (left ventricle, right ventricle)
• Elevations in CK-MB and Troponin I enzymes
• Myocardial contusion (trauma)
• Myocarditis
• Cardiomyopathy
• Post ischemic myocardial stunning
• Septic myocardial depression
• Pharmacologic
o Anthracycline cardiotoxicity
o Calcium channel blockers
21. Marc Imhotep Cray, M.D.
Distributive shock
21
Distributive shock results from excessive vasodilation
and impaired distribution of blood flow
• Septic shock is the most common form of
distributive shock and is characterized by
considerable mortality (treated, around 30%;
untreated, probably >80%)
• In United States, this is leading cause of
noncardiac death in intensive care units (ICUs)
22. Marc Imhotep Cray, M.D.
Distributive shock (2)
22
Other causes of distributive shock include systemic
inflammatory response syndrome (SIRS) due to
noninfectious inflammatory conditions such as burns and
pancreatitis; toxic shock syndrome (TSS); anaphylaxis;
reactions to drugs or toxins, including insect bites,
transfusion reaction, and heavy metal poisoning;
addisonian crisis; hepatic insufficiency; and neurogenic
shock due to brain or spinal cord injury
24. 24
Major pathogenic pathways in septic shock
Microbial products activate endothelial cells and cellular and humoral elements of the innate
immune system, initiating a cascade of events that lead to end-stage multiorgan failure.
DIC, Disseminated intravascular coagulation; HMGBI, high-mobility group box I protein; NO, nitric oxide; PAF, platelet-activating factor; PAI-I,
plasminogen activator inhibitor- I ; PAMP, pathogen- associated molecular pattern; STNFR, soluble tumor necrosis factor receptor; TF, tissue
factor; TFPI, tissue factor pathway inhibitor.
Robbins Basic Pathology 10e, Elsevier, 2018. Fig. 4.19, Pg. 117.
25. Marc Imhotep Cray, M.D.
Distributive shock (4) Capsule
25
Distributive shock
• As in hypovolemic shock, there is an insufficient
intravascular volume of blood
• This form of "relative" hypovolemia is result of
dilation of blood vessels which diminishes
systemic vascular resistance
• Examples of this form of shock are:
1. Septic shock
2. Anaphylactic shock
3. Neurogenic shock
26. Marc Imhotep Cray, M.D.
Obstructive shock
26
Obstructive shock
• In this situation flow of blood is obstructed which
impedes circulation and can result in circulatory
arrest
• Several conditions result in this form of shock, including:
1. Cardiac tamponade
2. Tension pneumothorax
3. pulmonary embolism
4. Aortic stenosis
27. Marc Imhotep Cray, M.D.
Extracardiac obstructive shock
Impaired diastolic filling (decreased preload)
27
High CVP, Low PCWP, Cardiac Output is usually decreased w increased SVR
• A physical impairment to adequate forward circulatory flow
involving mechanisms different than primary myocardial or
valvular dysfunction
• Frank decrease in filling pressures (as in mediastinal
compressions of great veins) or trends towards equalization of
pressures in case of cardiac tamponade or markedly increased
right ventricular filling pressures (Pulmonary arterial
hypertension [PAH])
28. Marc Imhotep Cray, M.D.
Endocrine shock
Recently a fifth form of shock has been introduced based
on endocrine disturbances.
28
Causes:
• Hypothyroidism, in critically ill patients, reduces cardiac output and
can lead to hypotension and respiratory insufficiency
• Thyrotoxicosis may induce a reversible cardiomyopathy
• Acute adrenal insufficiency is frequently the result of discontinuing
corticosteroid treatment without tapering the dosage
• However, surgery and intercurrent disease in patients on corticosteroid
therapy without adjusting dosage to accommodate for increased
requirements may also result in this condition
• Relative adrenal insufficiency in critically ill patients where present
hormone levels are insufficient to meet the higher demands
29. Marc Imhotep Cray, M.D.
Compensated vs.
decompensated shock
29
With compensated shock, body is experiencing a state of low blood
volume but is still able to maintain blood pressure and organ
perfusion by increasing heart rate and constricting blood vessels
Symptoms of compensated shock include:
Agitation, restlessness and anxiety
Altered mental status
Tachycardia or tachypnea
Change in pallor, cyanosis around the lips, or clammy skin
Nausea or vomiting
Thirst
Weak, thready or absent pulse
Narrowing pulse pressure
Shallow, rapid breathing
Mental status may be normal, in the early stages
30. Marc Imhotep Cray, M.D.
Compensated vs.
decompensated shock (2)
30
With compensated shock, body is able to take measures to maintain
blood pressure, however as shock worsens (decompensates), body
becomes unable to keep up perfusion of vital organs is no longer
maintained Lactic acidosis
Symptoms of decompensated shock include:
Falling blood pressure (systolic of 90 mm Hg or lower with adults)
Tachycardia and tachypnea
Low urine output
Labored and irregular breathing
Weak, thready or absent peripheral pulses
Ashy or cyanotic pallor
Reduced body temperature
Decreased mental status
Dilated pupils
31. Marc Imhotep Cray, M.D.
Decompensated shock
31
With decompensated shock, it may be necessary to request
advanced life support measures for patient
Priority should be given to management of airway and
treatment of the underlying cause of shock
A decrease in blood pressure is often an indication of late-
stage shock and treatment should start well before this is
detected
If condition remains untreated will progress into irreversible
shock ultimately leads to death
32. Marc Imhotep Cray, M.D.
Comparison of types of shock
(Early stage)
32
Vasoconstrictive Vasodilatative
Hypovolamic Cardiogenic Circulatory Septic
Cardiac
index
Cardiac
index
Peripheral
resistance
Peripheral
resistance
Blood
Volume
Blood
Volume
NB: Malperfusion and organ dysfunction
are ultimate end point of any shock stage
33. Marc Imhotep Cray, M.D. 33
Decreased cardiac output
Decreased blood pressure
Decreased tissue perfusion
Decreased coronary perfusion
Decreased myocardial function
Microcirculatory
obstruction
Cellular aggregation
Microcirculatory damage
Cell hypoxia
Metabolic
acidosis
Decreased
myocardial
contraction
Inracellular
fluid
loss
Decreased
venous return
BP = CO x SVR
Pathophysiology Concept Map
34. Marc Imhotep Cray, M.D.
Treating Shock Capsule
34
The key toward successfully treating shock is a rapid response
If it can be treated before reaching decompensated phase, that is
best
In many major life-threatening situations development of shock
should be anticipated
EM providers refer to a ‘golden hour’ or ‘golden period’ in which
care should be delivered as quickly as possible and if it is, patient
will not suffer any lasting damage requires a speedy assessment
of patient and rapid transport to a advance care facility
36. Marc Imhotep Cray, M.D.
Enhance compensatory phase of
shock
36
• Maintenance of mean circulatory pressure
• Maximizing cardiac function
• Redistributing perfusion to vital organs
• Optimizing unloading of oxygen at tissues
37. Marc Imhotep Cray, M.D.
Maintain Blood Volume
37
• Fluid redistribution to
vascular space
• From interstitium
(Starling effect)
• From intracellular
space (osmotic effect)
• Decreased renal fluid losses
• Decreased glomerular
filtration rate (GFR)
• Increased aldosterone
• Increased vasopressin
40. Marc Imhotep Cray, M.D.
Early mechanical ventilation
40
• allows blood flow to be redistributed
• tends to reverse lactic acidosis
• supports patient until other therapeutic measures
can be effective
Tidal volumes in order of 7-10 ml/kg of lean body mass, an
O2 concentration that results in arterial saturation not less
than 92%, adequate ventilator rate and sedation to minimize
the work of breathing.
41. Marc Imhotep Cray, M.D.
Fluid resuscitation
41
IV line c Large bore cannula
Choice of infusion
Sm. volume resuscitation (hypertonic NaCl solution)
General conditions: parameters ( BP, Pulse, CVP, SatO2 etc.)
Lactated Ringer's solution Colloids
Dextrane
Hydroethylstrach
Gelatine
43. Marc Imhotep Cray, M.D.
Summary of Shock
43
Shock is defined as a state of systemic tissue hypoperfusion
resulting from reduced cardiac output and/or reduced effective
circulating blood volume.
The major types of shock are cardiogenic (e.g., myocardial
infarction), hypovolemic (e.g., blood loss), and septic (e.g.,
infections).
Shock of any form can lead to hypoxic tissue injury if not
corrected.
Septic shock is caused by the host response to bacterial or fungal
infections; it is characterized by endothelial cell activation,
vasodilation, edema, disseminated intravascular coagulation, and
metabolic derangements.
45. Marc Imhotep Cray, M.D.
Further Study:
45
Reading:
Robbins Basic Pathology 10e, Elsevier, 2018 ;Pgs. 115-118.
Sethi, AK et al. Shock-A Short Review. Indian J. Anaesth.
2003; 47 (5) : 345-359
Video Lectures:
Circulatory Shock_Dr. Najeeb