Shock occurs when arterial blood flow is inadequate to meet metabolic needs, resulting from cardiovascular collapse. The main types are hypovolemic, cardiogenic, and distributive shock. Hypovolemic shock results from decreased intravascular volume due to blood, plasma, or fluid loss. Cardiogenic shock is caused by pump failure from myocardial damage or obstruction. Distributive shock reduces vascular resistance from sepsis, anaphylaxis, or SIRS. The body initially compensates for shock but decompensation occurs when mechanisms fail, potentially progressing to irreversible shock without treatment.
Properties of cm, plateau potential & pacemaker by Pandian M this PPT for I ...Pandian M
Describe the properties of cardiac muscle including its morphology, electrical, mechanical and metabolic functionsSLOs: After attending lecture & studying the assigned materials, the student will: 1.Describe the general features of cardiac muscle.2.Discuss the light and electron microscopic appearance of cardiac muscle, characteristic features of sarcotubular system.3.Enlist the electrical properties of heart muscle.4.Explain the phases of cardiac muscle action potential5.Explain the nodal action potential.6.Differentiate between cardiac muscle A.P. and nodal A.P., effect of nervous innervation and ions on AP.7.Enumerate and explain the mechanical properties of heart muscle, metabolic functions, characteristic features.
Regulation of arterial blood pressure (The Guyton and Hall Physiology)Maryam Fida
BLOOD PRESSURE
The pressure exerted by the blood on vessel wall is known as blood pressure.
SYSTOLIC BLOOD PRESSURE
The maximum pressure exerted in the arteries during systole of heart.
Normal systolic pressure: 120 mm Hg.
DIASTOLIC BLOOD PRESSURE
The minimum pressure exerted in the arteries during diastole of heart.
Normal diastolic pressure: 80 mm Hg.
PULSE PRESSURE
The difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
MEAN ARTERIAL BLOOD PRESSURE
The average pressure existing in the arteries.
Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
Pulse Pressure = (Systolic – Diastolic)
Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
Physiology of shock explains different kind of shock and their management. Made by Dr.Nitin Khajotia.
Septic shock
Cardiogenic shock
Anaphylactic shock
Septic shock (due to infections)
Neurogenic shock (caused by damage to the nervous system)
Signs and Symptom
management of shock general
Properties of cm, plateau potential & pacemaker by Pandian M this PPT for I ...Pandian M
Describe the properties of cardiac muscle including its morphology, electrical, mechanical and metabolic functionsSLOs: After attending lecture & studying the assigned materials, the student will: 1.Describe the general features of cardiac muscle.2.Discuss the light and electron microscopic appearance of cardiac muscle, characteristic features of sarcotubular system.3.Enlist the electrical properties of heart muscle.4.Explain the phases of cardiac muscle action potential5.Explain the nodal action potential.6.Differentiate between cardiac muscle A.P. and nodal A.P., effect of nervous innervation and ions on AP.7.Enumerate and explain the mechanical properties of heart muscle, metabolic functions, characteristic features.
Regulation of arterial blood pressure (The Guyton and Hall Physiology)Maryam Fida
BLOOD PRESSURE
The pressure exerted by the blood on vessel wall is known as blood pressure.
SYSTOLIC BLOOD PRESSURE
The maximum pressure exerted in the arteries during systole of heart.
Normal systolic pressure: 120 mm Hg.
DIASTOLIC BLOOD PRESSURE
The minimum pressure exerted in the arteries during diastole of heart.
Normal diastolic pressure: 80 mm Hg.
PULSE PRESSURE
The difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
MEAN ARTERIAL BLOOD PRESSURE
The average pressure existing in the arteries.
Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
Pulse Pressure = (Systolic – Diastolic)
Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
Physiology of shock explains different kind of shock and their management. Made by Dr.Nitin Khajotia.
Septic shock
Cardiogenic shock
Anaphylactic shock
Septic shock (due to infections)
Neurogenic shock (caused by damage to the nervous system)
Signs and Symptom
management of shock general
Physiology of shock explains different kind of shock and their management. Made by Dr.Nitin Khajotia.
Septic shock
Cardiogenic shock
Anaphylactic shock
Septic shock (due to infections)
Neurogenic shock (caused by damage to the nervous system)
Signs and Symptom
management of shock general
Animated slides doctor explains shock
SHOCK SYNDROMESHOCK SYNDROME
• Shock is a condition in which the cardiovascular system
fails to perfuse tissues adequately
• An impaired cardiac pump, circulatory system, and/or
volume can lead to compromised blood flow to tissues
• Inadequate tissue perfusion can result in:
– generalized cellular hypoxia (starvation)
– widespread impairment of cellular metabolism
– tissue damage organ failure
– death
ATHOPHYSIOLOGYPATHOPHYSIOLOGY
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death
Basics of Shock and its management. Compentency and SLO based learning for undergraduate medical training (MBBS)
Check out the lecture by clicking on the link below
https://www.youtube.com/watch?v=J5m4kh4FO7k
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
Stay informed, stay safe, and get your flu shot today!
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 Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
2. 2
The Physiology of ShockThe Physiology of Shock
R.E.B, 4MedStudents.com, 2003
3.
4. • Shock occurs when
the rate of arterial blood flow is inadequate to meet
metabolic tissue needs and is the consequence of
cardio-vascular collapse
• Essentials of diagnosis are
– Hypotension (<60 mmHG)
– Tachycardia
– Oliguria
– Altered mental status
– Peripheral hypoperfusion and hypoxia
5.
6. major types of shockmajor types of shock
• Hypovolemic shock
– Decreased intravascular volume resulting form loss of
blood, plasma, or fluids and electrolytes
• Cardiogenic shock
– Pump failure due to myocardial damage or massive
obstruction of outflow tracts
• Distributive shock
– Reduction of vascular resistance form
• Sepsis
• Anaphylaxis
• Systemic inflammatory response syndrome (SIRS)
• Hypovolemic shock
– Decreased intravascular volume resulting form loss of
blood, plasma, or fluids and electrolytes
• Cardiogenic shock
– Pump failure due to myocardial damage or massive
obstruction of outflow tracts
• Distributive shock
– Reduction of vascular resistance form
• Sepsis
• Anaphylaxis
• Systemic inflammatory response syndrome (SIRS)
7. Hypovolemic shock
(most common type of shock)
Hypovolemic shock
(most common type of shock)
• Loss of blood (hemorrhagic)
– External bleeding (wound to the outside or gastrointestinal)
– Internal bleeding (hematoma, hemothorax,
hemopertitoneum)
• Loss of plasma
– Burns
– Exfoliative dermatitis
• Loss of fluids and electrolytes
– External (vomiting, diarrhea, excessive sweating)
– Internal ( “third spacing” = pancreatitis, ascitis, bowl
obstruction
– Excessive sweating
8. Stages of hypovolemic shockStages of hypovolemic shock
• Mild (loss of < 20% blood volume)
– Few external signs in supine young patients but
• Increased capillary refill time ( longer 3 sec. = 10% volume loss)
• Moderate (loss of 20-40% blood volume)
– Patient becomes increasingly anxious and tachycardic >100 beats/min
(sympathetic response)
– oliguria
– blood pressure may be maintained in supine patient
• Severe (loss of > 40% blood volume)
– Classic signs of shock appear with hemodynamic instability
(Cave: if mental confusion occurs is an ominous clinical sign)
Only very short time frame may separate mild and severe shock
symptoms that lead, when left untreated, to progressive and
irreversible cell injury and death
• Mild (loss of < 20% blood volume)
– Few external signs in supine young patients but
• Increased capillary refill time ( longer 3 sec. = 10% volume loss)
• Moderate (loss of 20-40% blood volume)
– Patient becomes increasingly anxious and tachycardic >100 beats/min
(sympathetic response)
– oliguria
– blood pressure may be maintained in supine patient
• Severe (loss of > 40% blood volume)
– Classic signs of shock appear with hemodynamic instability
(Cave: if mental confusion occurs is an ominous clinical sign)
Only very short time frame may separate mild and severe shock
symptoms that lead, when left untreated, to progressive and
irreversible cell injury and death
9. Signs and Symptoms
• Low Blood Pressure
– Systolic BP is usually below 90 mmHg
• Pulse is rapid and weak
• Respiration is rapid and shallow
• Skin is pale, cool, and clammy
• Drowsiness
• Low Blood Pressure
– Systolic BP is usually below 90 mmHg
• Pulse is rapid and weak
• Respiration is rapid and shallow
• Skin is pale, cool, and clammy
• Drowsiness
10. Hypovolemic Shock
• Results from trauma in which there is blood
loss
• Decreased blood volume causes a decrease in
blood pressure
• Insufficient amounts of O2 is being transported
to body tissues and organs
Hypovolemic Shock
• Results from trauma in which there is blood
loss
• Decreased blood volume causes a decrease in
blood pressure
• Insufficient amounts of O2 is being transported
to body tissues and organs
11.
12.
13. Compensated Shock
• Early stages of shock where the body’s
compensatory mechanisms are able to
maintain normal perfusion
• Early stages of shock where the body’s
compensatory mechanisms are able to
maintain normal perfusion
14. Decompensated Shock
• Advanced stage of shock that occurs when the
body’s compensatory mechanisms fail to
maintain normal perfusion
• Advanced stage of shock that occurs when the
body’s compensatory mechanisms fail to
maintain normal perfusion
15. Irreversible Shock
• Stage of shock that has progressed to the point
that the body nor medical interventions correct
the problem
• Stage of shock that has progressed to the point
that the body nor medical interventions correct
the problem
16.
17.
18.
19.
20.
21.
22. Compensated and Decompensated
shock
• Usually the body is able to compensate but
when these mechanisms fail shock develops
and may progress
• Usually the body is able to compensate but
when these mechanisms fail shock develops
and may progress
23. Compensation Mechanisms
• Catecholamines may be secreted ( I.E.
Epinephrine and norepinephrine)
• The Renin-Angitensin system aids in
maintaining blood pressure
• Endocrine Response by pituitary gland results
in secretion of anti-diuretic hormone (ADH)
• Catecholamines may be secreted ( I.E.
Epinephrine and norepinephrine)
• The Renin-Angitensin system aids in
maintaining blood pressure
• Endocrine Response by pituitary gland results
in secretion of anti-diuretic hormone (ADH)
24. Catecholamine Release
• Epinephrine and Norepinephrine release
affects the cardiovascular system, causing
increase in HR, increase in Cardiac contractility
strength, arteriolar constriction which
elevates blood pressure
• Epinephrine and Norepinephrine release
affects the cardiovascular system, causing
increase in HR, increase in Cardiac contractility
strength, arteriolar constriction which
elevates blood pressure
25. Renin-Angiotensin system
• Renin is released from the kidneys and acts on
specialized plasma protein called
Angiotensinogen & produces Angiotensin I.
• Angiotensin I is converted to Angiotensin II by
enzymes in the lungs called Angiotensin
Converting Enzyme (ACE)
• Renin is released from the kidneys and acts on
specialized plasma protein called
Angiotensinogen & produces Angiotensin I.
• Angiotensin I is converted to Angiotensin II by
enzymes in the lungs called Angiotensin
Converting Enzyme (ACE)
26. Anti-Diuretic Hormone
• Causes the kidneys to reabsorb water creating
an additive to the aldostrone
• Causes the kidneys to reabsorb water creating
an additive to the aldostrone
27. Stages of ShockStages of Shock
• Initial non-progressive stage
– Baro-receptor reflexes
– Release of catecholamine
– Activation of renin-angiotensin-aldosteron system
– ADH release
results in tachycardia, peripheral vasoconstriction (cool skin) and renal fluid
conservation
• Progressive stage
– Widespread tissue hypoxia results in anaerobic glycolysis and
– Lactate acidosis (pH < 7.35)
– Vasodilation with blood pooling in microcirculation
– Declined cardiac output
– Oligouria
– Widespread tissue hypoxia
• Irreversible stage
– Widespread cell injury leading to
– Further decreased myocardial contractility
– Anuria with tubular necrosis
– Ischemic bowl may lead to leakage of bacterial flora
– Fluid in lung (ARDS)
28.
29.
30.
31.
32. S/S of Hypovolemic Shock
• Altered LOC
• Pale, cool, clammy skin
• Blood pressure may be normal then fall
• Pulse may be normal then become rapid, finally
slowing and disappearing
• Urination decreases
• Cardiac dysrhythmias may occur
• Altered LOC
• Pale, cool, clammy skin
• Blood pressure may be normal then fall
• Pulse may be normal then become rapid, finally
slowing and disappearing
• Urination decreases
• Cardiac dysrhythmias may occur
33. Tx for Hypovolemic Shock
• Airway control
• Administer high flow oxygen
• Control severe bleeding
• Keep patient warm
• Elevate lower extremities
• Establish IV and administer bolus of crystalloid
solution for fluid replacement
• Airway control
• Administer high flow oxygen
• Control severe bleeding
• Keep patient warm
• Elevate lower extremities
• Establish IV and administer bolus of crystalloid
solution for fluid replacement
34.
35.
36. Cardiogenic shockCardiogenic shock
• Pump failure
– Secondary to myocardial infarction (most common)
– Cardio-myophathy
– Acute valvular dysfunction (regurgitations)
– Rupture of the ventricular septum
• Arrhythmia
– Tachyarrhythmia
– Bradyarrhythmia
• Obstructions
– Tension pneumothorax
– Pericardial diseases (tamponade or constrictive pericarditis)
– Pulmonary hypertension (emboli or other vascular diseases)
37. Characteristics of Cardiogenic Shock
• Low cardiac output
• Peripheral vasoconstriction
• Left sided heart failure leads to pulmonary venous
congestion and pulmonary edema
• Right sided heart failure leads to systemic venous
congestion and peripheral edema
38. It is essential to distinguish a cardiogenic from a hypovolemic
shock!
Both forms are associated with reduced cardiac out put, and increased
peripheral vascular resistance, however:
It is essential to distinguish a cardiogenic from a hypovolemic
shock!
Both forms are associated with reduced cardiac out put, and increased
peripheral vascular resistance, however:
Cardiogenic shock:
jugular venous distention (high CVP)
Hypovolemic shock: collapsed
capacitance veins (low CVP)
Cardiogenic shock:
jugular venous distention (high CVP)
Hypovolemic shock: collapsed
capacitance veins (low CVP)
39. Cardiogenic Shock
• The heart loses the ability to supply all body
parts with blood
• Usually the result of left ventricular failure
secondary to acute MI or CHF
• Many patients will have normal blood
pressures
• The heart loses the ability to supply all body
parts with blood
• Usually the result of left ventricular failure
secondary to acute MI or CHF
• Many patients will have normal blood
pressures
40. S/S of Cardiogenic Shock
• Major difference between other types of shock
is presence of Pulmonary Edema
• Difficulty breathing
• Wheezes, Crackles, Rales are heard as fluid
levels increase
• Productive cough with white or pink-tinged
foamy sputum
• Cyanosis
• Altered mentation
• Oliguria ( decreased urination)
• Major difference between other types of shock
is presence of Pulmonary Edema
• Difficulty breathing
• Wheezes, Crackles, Rales are heard as fluid
levels increase
• Productive cough with white or pink-tinged
foamy sputum
• Cyanosis
• Altered mentation
• Oliguria ( decreased urination)
41. TX for Cardiogenic Shock
• Assure open airway
• Adminster oxygen
• Assist ventilations as needed
• Keep patient warm
• Place patient in position of comfort
• Establish Iv with minimal fluid administration
• Monitor Vitals
• May need to administer Dopamine or
Dobutamine
• Assure open airway
• Adminster oxygen
• Assist ventilations as needed
• Keep patient warm
• Place patient in position of comfort
• Establish Iv with minimal fluid administration
• Monitor Vitals
• May need to administer Dopamine or
Dobutamine
42. Distributive ShockDistributive Shock
• Sepsis
– Due to gram negative or gram positive bacteria
• Anaphylaxis
– Due to previous sensitization to an allergen
• Neurogenic
– Due to traumatic spinal cord injury
– Effects of epidural or spinal anesthetics
– Reflex parasymapthetic stimulation
• Sepsis
– Due to gram negative or gram positive bacteria
• Anaphylaxis
– Due to previous sensitization to an allergen
• Neurogenic
– Due to traumatic spinal cord injury
– Effects of epidural or spinal anesthetics
– Reflex parasymapthetic stimulation
43. Types of ShockTypes of Shock
Neurogenic Shock
• Results due to the overall dilation of the blood
vessels within the cardiovascular system
• Decreased blood pressure
• Insufficient amounts of O2 is being transported
to body tissues and organs
Neurogenic Shock
• Results due to the overall dilation of the blood
vessels within the cardiovascular system
• Decreased blood pressure
• Insufficient amounts of O2 is being transported
to body tissues and organs
44.
45.
46. Neurogenic Shock
• Results from injury to brain or spinal cord
causing interruption of nerve impulses to
arteries
• Arteries lose tone and dilate causing
hypovolemia
• Sympathetic nerve impulses to the adrenal
glands are lost, which prevents the release of
catecholamines and their compensatory effects
• Results from injury to brain or spinal cord
causing interruption of nerve impulses to
arteries
• Arteries lose tone and dilate causing
hypovolemia
• Sympathetic nerve impulses to the adrenal
glands are lost, which prevents the release of
catecholamines and their compensatory effects
47. Neurogenic Shock (con’t)
• High cervical injuries cause interruption of
impulse to peripheral nervous system causing
• Neurogenic shock is most commonly due to
severe injury to spinal cord or total transection
of cord (spinal shock)
• High cervical injuries cause interruption of
impulse to peripheral nervous system causing
• Neurogenic shock is most commonly due to
severe injury to spinal cord or total transection
of cord (spinal shock)
48. S/S of Neurogenic Shock
• Warm, Dry, Red Skin
• Low Blood Pressure
• Slow Pulse
• Warm, Dry, Red Skin
• Low Blood Pressure
• Slow Pulse
49. TX for Neurogenic Shock
• Airway control
• Maintain body temperature
• Immobilization if indicated
• Consider other causes of shock
• IV and medications that increase peripheral
vascular resistance (I.E. Norepinephrine,
Dopamine)
• Airway control
• Maintain body temperature
• Immobilization if indicated
• Consider other causes of shock
• IV and medications that increase peripheral
vascular resistance (I.E. Norepinephrine,
Dopamine)
50.
51.
52. Anaphylatic Shock
• Severe immune response to foreign substance
• S/S most often occur within minutes but can
take up to hours to occur
• The faster the reaction develops the more
severe it is likely to be
• Death will occur if not treated promptly
• Severe immune response to foreign substance
• S/S most often occur within minutes but can
take up to hours to occur
• The faster the reaction develops the more
severe it is likely to be
• Death will occur if not treated promptly
57. S/S of Anaphylactic Shock
• Gastrointestinal System
- Nausea, vomiting
- Abdominal cramping
- Diarrhea
• Gastrointestinal System
- Nausea, vomiting
- Abdominal cramping
- Diarrhea
58. TX for Anaphylactic Shock
• Airway protection which may include
Endotracheal Intubation
• Establish IV with crystalloid solution
• Pharmacological interventions: Epinephrine,
Antihistamines(Benadryl),
Corticosteroids(dexamethasone),
Vasopressors(dopamine, Epinephrine), and
inhaled beta agonist(albuterol)
• Airway protection which may include
Endotracheal Intubation
• Establish IV with crystalloid solution
• Pharmacological interventions: Epinephrine,
Antihistamines(Benadryl),
Corticosteroids(dexamethasone),
Vasopressors(dopamine, Epinephrine), and
inhaled beta agonist(albuterol)
59.
60.
61. Pathogenesis of Septic Shock
(vasodilatory shock)
• Sepsis is defined as a systemic inflammatory response
to a bacterial infection with bacteriemia (though
blood cultures can be negative)
• Severe sepsis is defined by additional end-organ
dysfunction (mortality rate: 25-30%)
• Septic shock is defined as sepsis with hypotension
despite fluid resuscitation and evidence of inadequate
tissue perfusion (40-70%)
• Sepsis is defined as a systemic inflammatory response
to a bacterial infection with bacteriemia (though
blood cultures can be negative)
• Severe sepsis is defined by additional end-organ
dysfunction (mortality rate: 25-30%)
• Septic shock is defined as sepsis with hypotension
despite fluid resuscitation and evidence of inadequate
tissue perfusion (40-70%)
64. Clinical Spectrum of Infection
Infection
Sepsis
Severe Sepsis
Septic Shock
Bacteremia
65.
66. The syndrome of septic shock is characterized
by
• Systemic vasodilation (hypotension)
• Diminished myocardial contractility
• Widespread endothelial injury and activation leading
to fluid leakage (capillary leak) resulting in acute
respiratory distress syndrome (ARDS)
• Activation of the coagulation cascade (DIC)
• Systemic vasodilation (hypotension)
• Diminished myocardial contractility
• Widespread endothelial injury and activation leading
to fluid leakage (capillary leak) resulting in acute
respiratory distress syndrome (ARDS)
• Activation of the coagulation cascade (DIC)
67.
68. Disseminated intravascular coagulation (DIC)
• is characterized by widespread activation of coagulation
resulting in the intravascular formation of fibrin and ultimately
thrombotic occlusion of small and midsize vessels
• leads to compromise of blood supply to organs and may
therefore contribute to multiple organ failure
• subsequent depletion of platelets and coagulation factors can
result in severe bleeding and may be the presenting symptom
• is characterized by widespread activation of coagulation
resulting in the intravascular formation of fibrin and ultimately
thrombotic occlusion of small and midsize vessels
• leads to compromise of blood supply to organs and may
therefore contribute to multiple organ failure
• subsequent depletion of platelets and coagulation factors can
result in severe bleeding and may be the presenting symptom
69. Virtually all patients with sepsis have coagulation
abnormalities. The extreme form of it is called:
Acute disseminated intravascular coagulation (DIC)
Severe cutaneous bleeding as a result of fulminant Meningococcal
septicemia due to activation and consumption of all coagulation
factors (consumption coagulopathy)
70.
71. Septic Shock
• An infection enters bloodstream and is carried
throughout body
• Toxins released overcome compensatory
mechanisms
• Can cause dysfunction of one organ system or
cause multiple organ dysfunction
• An infection enters bloodstream and is carried
throughout body
• Toxins released overcome compensatory
mechanisms
• Can cause dysfunction of one organ system or
cause multiple organ dysfunction
72. S/S of Septic Shock
• Increased to low blood pressure
• High fever, no fever, hypothermic
• Skin flushed, Pale, Cyanotic
• Difficulty breathing and altered lung sounds
• Altered LOC
• Increased to low blood pressure
• High fever, no fever, hypothermic
• Skin flushed, Pale, Cyanotic
• Difficulty breathing and altered lung sounds
• Altered LOC
73. TX of Septic Shock
• Airway control
• Administer oxygen
• IV of crystalloid solution
• Dopamine for blood pressure support
• Monitor other vitals
• Airway control
• Administer oxygen
• IV of crystalloid solution
• Dopamine for blood pressure support
• Monitor other vitals
Editor's Notes
Septic shock is a continuumalong this pathway of worsening of microorganisms in normally sterile host tissues and their ongoing invasion.
Infection- the presence of microorganisms in normally sterile host tissue.
Bacteremia- the presence of viable bacteria in blood
Sepsis- The systemic response to infection
Severe sepsis- sepsis associated with organ dysfunction, hypoperfusion or hypotension.
Septic shock- sepsis with hypotension despite adequate fluid resuscitation, and perfusion abnormalitites.
71% of patients with culture proven septic shock are initially identified as being in one of the milder categories, yet only 4% of patients with SIRS progress to full septick shock.
Rangel-Fausto MS, Pittet D, Castigan M, Hwang T, et al., The natural history of the systemic inflammatory response syndrome. JAMA 1995; 273: 117-123.
Its important to identify these patients early when they are more amenable to succsessful intervention.