IVUS may not be clinically warranted in all interventions, and should be seen as an adjunct to angiography. IVUS provides information about vessel morphology, plaque topography, and therapeutic outcomes that is often either equivocal or unavailable in angiographic images.
There are 3 situations in which IVUS has the most clinical utility:
Small vessel stenting: Studies have shown that post-stent restenosis rates are higher in small vessels. This is particularly true for vessels with diameters of 3.0mm or less, wherein small increases in stent diameter have been shown to significantly decrease the rate of restenosis. A study by Moussa et al showed that, as measured by IVUS, the incidence of restenosis has an inverse relationship to the post-procedure in-stent lumen CSA1.
In-Stent restenosis: In these cases, IVUS helps to determine whether the restenosis is due to inadequate stent deployment (underexpansion or incomplete apposition) due to intimal hyperplasia. IVUS will also help you select the proper device size for treatment of the stented area.
Difficult to assess lesions: At times, images of a lesion and the adjacent reference segment are often hazy. IVUS should be used to identify whether the angiographic appearance is due to dissection, thrombus, residual plaque, or is benign.
IVUS may not be clinically warranted in all interventions, and should be seen as an adjunct to angiography. IVUS provides information about vessel morphology, plaque topography, and therapeutic outcomes that is often either equivocal or unavailable in angiographic images.
There are 3 situations in which IVUS has the most clinical utility:
Small vessel stenting: Studies have shown that post-stent restenosis rates are higher in small vessels. This is particularly true for vessels with diameters of 3.0mm or less, wherein small increases in stent diameter have been shown to significantly decrease the rate of restenosis. A study by Moussa et al showed that, as measured by IVUS, the incidence of restenosis has an inverse relationship to the post-procedure in-stent lumen CSA1.
In-Stent restenosis: In these cases, IVUS helps to determine whether the restenosis is due to inadequate stent deployment (underexpansion or incomplete apposition) due to intimal hyperplasia. IVUS will also help you select the proper device size for treatment of the stented area.
Difficult to assess lesions: At times, images of a lesion and the adjacent reference segment are often hazy. IVUS should be used to identify whether the angiographic appearance is due to dissection, thrombus, residual plaque, or is benign.
EMBOLISM AND FILTERS USED IN CARDIOPULMONARY BYPASSGLORY MINI MOL. A
FILTERS USED IN CARDIOPULMONARY BYPASS
EMBOLISM
DEFINITION: obstruction of an artery, by a clot of blood or an air bubble.
This emboli is categorized to
Biological emboli
Foreign emboli
Gaseous emboli
There are current technologies to decrease this embolic event delivered to patient
Membrane oxygenators
FILTER
Blood surface coating
Bubble traps
Emboli detection system
Blood Filters
Depth filters
Consist of packed fibers of Dacron wool or
polyurethane foam .
No defined pore size
These filters have large wetted surface
areas to filter the blood by absorption , they are effective in
trapping gross bubbles.
Screen filters
composed of a woven
mesh of polyester fibers
defined pore sizes
From 20 -40 μm
(all of the arterial line filters used are the screen type)
Chronic Total Occlusions: The Road Less TraveledAllina Health
By M. Nicholas Burke, MD. The use of pioneering percutaneous treatments for chronic total occlusions: indications, limitations, outcomes and current research.
Survival in patients with advanced heart failure (AHF) has improved over the last 2 decades. An increasing number of patients however, are dying with progressive heart failure over the same duration. Optimal utilization of medical therapies and devices like implantable defibrillators and biventricular pacemakers are the likely reasons patients are surviving longer albeit with progressive HF.
Evolution in mechanical circulatory support (MCS) devices has occurred over the same period, such that they can now be rapidly instituted providing support for pump failure, often percutaneously, with timely restitution of physiologic and metabolic derangements with fewer complications.
MCS devices can be classified as Short term and Long term. Short term devices such as Intraaortic balloon pumps (IABP), Impella ®, TandemHeart® or Venoarterial extracorporeal membrane oxygenation (VA – ECMO) using a Cardiohelp® device, are usually employed as ‘Bridge to Recovery’(BTR) or Bridge to Decision’(BTD), usually in acute settings. Long term devices such as implantable left ventricular assist devices (LVADs) e.g. Heartmate II® & 3®, Heart ware HVAD® are implanted as ‘Bridge to transplant’ (BTT) or ‘Destination therapy’ (DT) usually in patients ‘sliding’ on inotropes when they are transplant eligible (BTT) or ineligible (DT) respectively.
Ventricular assist devices have traditionally been developed for left ventricular support in case of severe left heart or biventricular dysfunction. Historically, right ventricular (RV) dysfunction following LVAD implantation or as a component of biventricular dysfunction was managed with either medical therapy, temporary VADs (i.e. ECMO configuration with continuous flow centrifugal pumps like CentriMag®, Rotaflow ®) or occasionally with LVADs placed on the right side. Recently the Impella RP® and ProtekDuo®, percutaneously placed pumps with inflow in the inferior vena cava & right atrium respectively and outflow in pulmonary artery, have become available as less invasive options, for short term RV support.
The Syncardia® is the only approved total artificial heart system currently in use; however various biventricular, total heart systems (e.g. BiVACOR®) in development show promise.
Mechanical circulatory devices provide attractive, viable, physiologically plausible ventricular support options that can be used effectively in carefully selected patients.
"Shock" is a multifaceted condition that can range from being mild to extremely fatal. This is a condition whose knowledge is a must for medical practitioners; especially the one in the field of Dentistry.
its sometime difficult to decide in urgent clinical scenarios - Trauma,active bleeding, surgery: What ; when ; how and why to transfuse? answering some of these queries here is my presentation especially made for PG students (will help in answer writing)
EMBOLISM AND FILTERS USED IN CARDIOPULMONARY BYPASSGLORY MINI MOL. A
FILTERS USED IN CARDIOPULMONARY BYPASS
EMBOLISM
DEFINITION: obstruction of an artery, by a clot of blood or an air bubble.
This emboli is categorized to
Biological emboli
Foreign emboli
Gaseous emboli
There are current technologies to decrease this embolic event delivered to patient
Membrane oxygenators
FILTER
Blood surface coating
Bubble traps
Emboli detection system
Blood Filters
Depth filters
Consist of packed fibers of Dacron wool or
polyurethane foam .
No defined pore size
These filters have large wetted surface
areas to filter the blood by absorption , they are effective in
trapping gross bubbles.
Screen filters
composed of a woven
mesh of polyester fibers
defined pore sizes
From 20 -40 μm
(all of the arterial line filters used are the screen type)
Chronic Total Occlusions: The Road Less TraveledAllina Health
By M. Nicholas Burke, MD. The use of pioneering percutaneous treatments for chronic total occlusions: indications, limitations, outcomes and current research.
Survival in patients with advanced heart failure (AHF) has improved over the last 2 decades. An increasing number of patients however, are dying with progressive heart failure over the same duration. Optimal utilization of medical therapies and devices like implantable defibrillators and biventricular pacemakers are the likely reasons patients are surviving longer albeit with progressive HF.
Evolution in mechanical circulatory support (MCS) devices has occurred over the same period, such that they can now be rapidly instituted providing support for pump failure, often percutaneously, with timely restitution of physiologic and metabolic derangements with fewer complications.
MCS devices can be classified as Short term and Long term. Short term devices such as Intraaortic balloon pumps (IABP), Impella ®, TandemHeart® or Venoarterial extracorporeal membrane oxygenation (VA – ECMO) using a Cardiohelp® device, are usually employed as ‘Bridge to Recovery’(BTR) or Bridge to Decision’(BTD), usually in acute settings. Long term devices such as implantable left ventricular assist devices (LVADs) e.g. Heartmate II® & 3®, Heart ware HVAD® are implanted as ‘Bridge to transplant’ (BTT) or ‘Destination therapy’ (DT) usually in patients ‘sliding’ on inotropes when they are transplant eligible (BTT) or ineligible (DT) respectively.
Ventricular assist devices have traditionally been developed for left ventricular support in case of severe left heart or biventricular dysfunction. Historically, right ventricular (RV) dysfunction following LVAD implantation or as a component of biventricular dysfunction was managed with either medical therapy, temporary VADs (i.e. ECMO configuration with continuous flow centrifugal pumps like CentriMag®, Rotaflow ®) or occasionally with LVADs placed on the right side. Recently the Impella RP® and ProtekDuo®, percutaneously placed pumps with inflow in the inferior vena cava & right atrium respectively and outflow in pulmonary artery, have become available as less invasive options, for short term RV support.
The Syncardia® is the only approved total artificial heart system currently in use; however various biventricular, total heart systems (e.g. BiVACOR®) in development show promise.
Mechanical circulatory devices provide attractive, viable, physiologically plausible ventricular support options that can be used effectively in carefully selected patients.
"Shock" is a multifaceted condition that can range from being mild to extremely fatal. This is a condition whose knowledge is a must for medical practitioners; especially the one in the field of Dentistry.
its sometime difficult to decide in urgent clinical scenarios - Trauma,active bleeding, surgery: What ; when ; how and why to transfuse? answering some of these queries here is my presentation especially made for PG students (will help in answer writing)
Cardiogenicshock by Dr.Afroza Prioty -140123092109-phpapp02Afroza Prioty
A small overview on cardiogenic shock which sometimes becomes a burning issue for the medical personnels and to combat the situation, the measures should be taken immediately and urgently.
A very narrative discussion over Shock & Haemorrhage, Blood Transfusion, Blood Products which is presented in seminers. A concise guideline of a vast chapter.
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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.
Stay informed, stay safe, and get your flu shot today!
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
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Shock
1. Presented by: Dr. Mashfiqul HasanPresented by: Dr. Mashfiqul Hasan
EmOC (anaesthesia) traineeEmOC (anaesthesia) trainee
ICMHICMH
2. Shock is a state of wide spread tissueShock is a state of wide spread tissue
hypo perfusion caused byhypo perfusion caused by
an inadequate cardiac output oran inadequate cardiac output or
ineffective circulatory blood volume,ineffective circulatory blood volume,
leading to inadequate supply of oxygenleading to inadequate supply of oxygen
and nutrients to the tissues and removal ofand nutrients to the tissues and removal of
metabolic wastes from there to the organsmetabolic wastes from there to the organs
of excretion.of excretion.
What isWhat is shock ?shock ?What isWhat is shock ?shock ?
3. Shock caused by inadequate cardiacShock caused by inadequate cardiac
outputoutput
CO = SV x HRCO = SV x HR
4. Stroke
Volum
e
Stroke VolumeStroke Volume
Volume of Blood pumped by eachVolume of Blood pumped by each
ventricle during 1 cardiac cycle.ventricle during 1 cardiac cycle.
What affects Stroke volume?
Heart
Muscle
Damag
e
Blood
Volume
Mechanica
lObstructi
on
Mechanic
al
Rhythm
Problems
6. Shock due to ineffective circulatoryShock due to ineffective circulatory
blood volumeblood volume
BP = CO x SVRBP = CO x SVR
7. Stages of shockStages of shock
Non progressive stageNon progressive stage
Progressive stageProgressive stage
Irreversible stageIrreversible stage
8. Classification of shockClassification of shock
Hypovolemic shockHypovolemic shock
Cardiogenic shockCardiogenic shock
Distributive shockDistributive shock
Obstructive shockObstructive shock
9. Hypovolemic shockHypovolemic shock
Loss of blood:Loss of blood:
External hemorrhage: trauma(accidental, surgical), GIExternal hemorrhage: trauma(accidental, surgical), GI
bleeding, PV bleedingbleeding, PV bleeding
Internal hemorrhage: hemothorax, hemoperitoneum,Internal hemorrhage: hemothorax, hemoperitoneum,
hematoma, haemorrhage due to pelvic bone fracture,hematoma, haemorrhage due to pelvic bone fracture,
femur fracture, etc.femur fracture, etc.
Loss of plasma: burn, exfoliative dermatitisLoss of plasma: burn, exfoliative dermatitis
Loss of fluid & electrolytes:Loss of fluid & electrolytes:
External: diarrhoea, vomiting, excessive sweating,External: diarrhoea, vomiting, excessive sweating,
hyperosmolar state (DKA, HONKDC)hyperosmolar state (DKA, HONKDC)
Internal: pancreatitis, ascites, bowel obstructionInternal: pancreatitis, ascites, bowel obstruction
10. Effect of hemorrhage on cardiacEffect of hemorrhage on cardiac
output & blood pressureoutput & blood pressure
100%100%
50%50%
00 1010 2020 3030 4040 5050
ArterialArterial pressurepressure
Cardiac outputCardiac output
Percentage of total blood removedPercentage of total blood removed
11. What prevented fall of bloodWhat prevented fall of blood
pressure?pressure?
Reflex sympathetic compensation:Reflex sympathetic compensation:
Arterioles constrict, increasing peripheral resistanceArterioles constrict, increasing peripheral resistance
Vein & venous reservoirs constrict (esp. skin &Vein & venous reservoirs constrict (esp. skin &
splanchnic), thereby increasing the venous returnsplanchnic), thereby increasing the venous return
Stimulation of the cardiac activityStimulation of the cardiac activity
Activation of Renin-Angiotensin-AldosteroneActivation of Renin-Angiotensin-Aldosterone
systemsystem
Formation and release of vasopressinFormation and release of vasopressin
12. Decreased cardiac outputDecreased cardiac output
Decreased arterial pressureDecreased arterial pressure
Decreased systemic blood flowDecreased systemic blood flow
Decreased nutrition of tissuesDecreased nutrition of tissues Intravascular clottingIntravascular clottingDecreased cardiac nutritionDecreased cardiac nutrition
Decreased nutritionDecreased nutrition
of vascular systemof vascular system
Decreased nutritionDecreased nutrition
of the brainof the brain
Tissue ischemiaTissue ischemia
Decreased vasomotorDecreased vasomotor
activityactivity
Vascular dilatationVascular dilatation
Venous poolingVenous pooling
Of bloodOf blood
Cardiac depressionCardiac depression Decreased venous returnDecreased venous return
IncreasedIncreased
CapillaryCapillary
permeabilitypermeability
DecreasedDecreased
blood volumeblood volume
Release ofRelease of
Toxins/lactic acidosisToxins/lactic acidosis
Progression of shockProgression of shock
14. Classification of HaemorrhageClassification of Haemorrhage
Class-I: Blood loss 15%Class-I: Blood loss 15%
Normal pulse rate and blood pressureNormal pulse rate and blood pressure
Tilt test +Tilt test +
Class-II: Blood loss 20-25%Class-II: Blood loss 20-25%
Tachycardia, TachypnoeaTachycardia, Tachypnoea
Low systolic blood pressureLow systolic blood pressure
Pulse pressure less than 30mmHgPulse pressure less than 30mmHg
Delayed capillary fillingDelayed capillary filling
Class-III: Blood loss 30-35%Class-III: Blood loss 30-35%
Skin-cold, clammy and paleSkin-cold, clammy and pale
Severe drop in blood pressureSevere drop in blood pressure
Restlessness, oliguria, metabolic acidosisRestlessness, oliguria, metabolic acidosis
Class-IV Blood loss 40-50%Class-IV Blood loss 40-50%
Profound hypotensionProfound hypotension
Carotid pulse may only be palpableCarotid pulse may only be palpable
Irreversible shockIrreversible shock
15. DiagnosisDiagnosis
HistoryHistory
Physical signs of haemodynamic instabilityPhysical signs of haemodynamic instability
The diagnosis is more difficult when theThe diagnosis is more difficult when the
source of blood loss is occult, as into thesource of blood loss is occult, as into the
gastrointestinal tract, fracture of femur,gastrointestinal tract, fracture of femur,
pelvic fracture or when plasma volumepelvic fracture or when plasma volume
alone is depleted.alone is depleted.
16. MonitoringMonitoring
Patients in shock require care in an intensivePatients in shock require care in an intensive
care unit.care unit.
Arterial pressure through an indwelling line,Arterial pressure through an indwelling line,
pulse, and respiratory rate should be monitoredpulse, and respiratory rate should be monitored
continuously;continuously;
A Foley catheter should be inserted to followA Foley catheter should be inserted to follow
urine flow;urine flow;
Mental status should be assessed frequently.Mental status should be assessed frequently.
Invasive monitoring: Pulmonary artery catheterInvasive monitoring: Pulmonary artery catheter
(PAC, Swan-Ganz catheter).(PAC, Swan-Ganz catheter).
17. Hemodynamic ParametersHemodynamic Parameters
CVP & PCWP CO SVR
Cardiogenic High Low High
Extra-cardiac
obstructive (Low) Low High
Hypovolemic Low Low High
Sepsis Variable Variable Low
Toxic Shock (Low) (High) Low
Anaphylaxis Low High Low
18. Management of hypovoloemic shockManagement of hypovoloemic shock
Irrespective of etiology the first treatment ofIrrespective of etiology the first treatment of
shock is 100%Oshock is 100%O22 inhalation.inhalation.
Initial resuscitation requires rapid re-expansionInitial resuscitation requires rapid re-expansion
of the circulating intravascular volume andof the circulating intravascular volume and
interventions to control ongoing losses.interventions to control ongoing losses.
Volume resuscitation is initiated with the rapidVolume resuscitation is initiated with the rapid
infusion of a balanced salt solution such asinfusion of a balanced salt solution such as
Ringer's lactate or Normal saline through large-Ringer's lactate or Normal saline through large-
bore intravenous lines.bore intravenous lines.
No distinct benefit from the use of colloid hasNo distinct benefit from the use of colloid has
been demonstrated & in some studies theybeen demonstrated & in some studies they
seem to be even harmful.seem to be even harmful.
19. Hypovolemic Shock - Fluid SelectionHypovolemic Shock - Fluid Selection
Distribution % Intravascular
Normal saline Extracellular space 25-30%
Lactated Ringer’s Extracellular space 25-30%
5% DA Total body water space 8-10%
Blood/ Colloids Intravascular space 100%
21. Aims of therapyAims of therapy
To achieve and maintainTo achieve and maintain
MAP of 70-80 mm of HgMAP of 70-80 mm of Hg
Urine output >0.5 ml/kg/hourUrine output >0.5 ml/kg/hour
Treatment of the cause.Treatment of the cause.
22. Further managementFurther management
Continuing blood loss, with hemoglobinContinuing blood loss, with hemoglobin
concentrations declining to 10 g/dL shouldconcentrations declining to 10 g/dL should
initiate blood transfusion, cross-matched wholeinitiate blood transfusion, cross-matched whole
blood.blood.
In the presence of severe and/or prolongedIn the presence of severe and/or prolonged
hypotension, inotropic support with dopamine,hypotension, inotropic support with dopamine,
vasopressin, or dobutaminevasopressin, or dobutamine may bemay be required torequired to
maintain adequate ventricular performancemaintain adequate ventricular performance
afterafter blood volume has been restored.blood volume has been restored.
Once hemorrhage is controlled and the patientOnce hemorrhage is controlled and the patient
has been stabilized, blood transfusions may nothas been stabilized, blood transfusions may not
be continued unless the hemoglobin is <~7g/dLbe continued unless the hemoglobin is <~7g/dL
25. Hemodynamic ParametersHemodynamic Parameters
CVP & PCWP CO SVR
Cardiogenic High Low High
Extra-cardiac
obstructive (Low) Low High
Hypovolemic Low Low High
Sepsis Variable Variable Low
Toxic Shock (Low) (High) Low
Anaphylaxis Low High Low
26. ManagementManagement
Adjusting volume status to a level thatAdjusting volume status to a level that
ensures optimum LV filling pressure.ensures optimum LV filling pressure.
Use of ionotropic drugs.Use of ionotropic drugs.
27. Hemodynamic effects ofHemodynamic effects of
adrenoceptor subtypesadrenoceptor subtypes
TypeType TissueTissue ActionsActions
AlphaAlpha Most vascular smoothMost vascular smooth
musclemuscle
ContractionContraction
Beta 1Beta 1 HeartHeart Increases force & rate ofIncreases force & rate of
contractioncontraction
Beta 2Beta 2 Vascular smoothVascular smooth
musclemuscle
RelaxationRelaxation
D 1D 1 Smooth muscleSmooth muscle Dilates renal blood vesselsDilates renal blood vessels
AdrenalineAdrenaline NoradrenalineNoradrenaline DobutamineDobutamine DopamineDopamine
32. Septic shockSeptic shock
Sepsis with hypotension (arterial blood pressure <90Sepsis with hypotension (arterial blood pressure <90
mmHg systolic, or 40 mmHg less than patient's normalmmHg systolic, or 40 mmHg less than patient's normal
blood pressure) for at least 1 h despite adequate fluidblood pressure) for at least 1 h despite adequate fluid
resuscitation;resuscitation;
oror
Need for vasopressors to maintain systolic bloodNeed for vasopressors to maintain systolic blood
pressure 90 mmHgpressure 90 mmHg oror mean arterial pressure 70 mmHgmean arterial pressure 70 mmHg
33.
34.
35. Features of Septic Shock
High Cardiac OutputHigh Cardiac Output
Low Systemic Vascular ResistanceLow Systemic Vascular Resistance
Myocardial DysfunctionMyocardial Dysfunction
Hypovolemia as Ongoing CirculatingHypovolemia as Ongoing Circulating
Volume Lost To Interstitial SpaceVolume Lost To Interstitial Space
36.
37. General managementGeneral management
Measure CVPMeasure CVP If CVP is <8 mm of Hg – fluid is infusedIf CVP is <8 mm of Hg – fluid is infused
to raise it to 8-12 mm of Hgto raise it to 8-12 mm of Hg
Measure MAPMeasure MAP If MAP is still <65 mm of HgIf MAP is still <65 mm of Hg
- use vasoactive agent- use vasoactive agent
Maintain MAP >65 mm of HgMaintain MAP >65 mm of Hg
Management of septic shockManagement of septic shock
38. Neurogenic ShockNeurogenic Shock
Neurogenic shock is caused by-Neurogenic shock is caused by-
traumatic spinal cord injury ortraumatic spinal cord injury or
effects of an epidural or spinal anesthetic.effects of an epidural or spinal anesthetic.
This results in loss of sympathetic tone with a reductionThis results in loss of sympathetic tone with a reduction
in systemic vascular resistance and hypotension withoutin systemic vascular resistance and hypotension without
a compensatory tachycardia.a compensatory tachycardia.
The extremities are often warm, in contrast to the usualThe extremities are often warm, in contrast to the usual
vasoconstriction-induced coolness in hypovolemic orvasoconstriction-induced coolness in hypovolemic or
cardiogenic shock.cardiogenic shock.
Reflex vagal parasympathetic stimulation evoked byReflex vagal parasympathetic stimulation evoked by
pain, gastric dilation, or fright may simulate neurogenicpain, gastric dilation, or fright may simulate neurogenic
shock, producing hypotension, bradycardia, andshock, producing hypotension, bradycardia, and
syncope.syncope.
39. Management of neurogenic shockManagement of neurogenic shock
Treatment involves a simultaneous approach toTreatment involves a simultaneous approach to
the relative hypovolemia and to the loss ofthe relative hypovolemia and to the loss of
vasomotor tone.vasomotor tone.
Excessive volumes of fluid may be required toExcessive volumes of fluid may be required to
restore normal hemodynamics if given alone.restore normal hemodynamics if given alone.
A pure alpha-adrenergic agentA pure alpha-adrenergic agent
(Ephedrine/phenylephrine) may be necessary to(Ephedrine/phenylephrine) may be necessary to
augment vascular resistance and maintain anaugment vascular resistance and maintain an
adequate mean arterial pressure.adequate mean arterial pressure.
In severe cases noradrenaline/adrenaline mayIn severe cases noradrenaline/adrenaline may
be used.be used.
40. Anaphylactic shockAnaphylactic shock
Anaphylaxis is a potentially life-Anaphylaxis is a potentially life-
threatening, systemic allergic reactionthreatening, systemic allergic reaction
caused by the release of histamine andcaused by the release of histamine and
other vasoactive mediators.other vasoactive mediators.
The most common allergens are foods,The most common allergens are foods,
latex, insect venom and drugs.latex, insect venom and drugs.
41.
42. Anaphylaxis: IgE-mediatedAnaphylaxis: IgE-mediated
mast cell degranulationmast cell degranulation
FoodsFoods
PeanutsPeanuts
Tree nutsTree nuts
Fish and shellfishFish and shellfish
MilkMilk
EggsEggs
Soy productsSoy products
Insect stingsInsect stings
Bee venomBee venom
Wasp venomWasp venom
Chemicals, drugs and other foreign proteinsChemicals, drugs and other foreign proteins
Penicillin and other antibioticsPenicillin and other antibiotics
Intravenous anaesthetic agents, e.g. suxamethonium, propofolIntravenous anaesthetic agents, e.g. suxamethonium, propofol
LatexLatex
43. Anaphylactoid, non-IgE-mediatedAnaphylactoid, non-IgE-mediated
mast cell degranulationmast cell degranulation
DrugsDrugs
OpiatesOpiates
AspirinAspirin
Radiocontrast mediaRadiocontrast media
PhysicalPhysical
ExerciseExercise
ColdCold
IdiopathicIdiopathic
No cause can be identified in 30% of patients withNo cause can be identified in 30% of patients with
anaphylaxisanaphylaxis
44. Management of anaphylaxisManagement of anaphylaxis
Anaphylaxis is an acute medical emergency. TheAnaphylaxis is an acute medical emergency. The
immediate management includes:immediate management includes:
preventing further contact with the allergen (e.g. removal of beepreventing further contact with the allergen (e.g. removal of bee
sting)sting)
ensuring airway patencyensuring airway patency
administration of oxygenadministration of oxygen
restoration of blood pressure (laying the patient flat, intravenousrestoration of blood pressure (laying the patient flat, intravenous
fluids)fluids)
prompt administration of adrenaline (epinephrine).prompt administration of adrenaline (epinephrine).
Intravenous antihistamines (chlorphenamine 10-20 mg i.m. orIntravenous antihistamines (chlorphenamine 10-20 mg i.m. or
slow i.v. injection), which limit ongoing inflammation.slow i.v. injection), which limit ongoing inflammation.
Corticosteroids (hydrocortisone 100-300 mg) prevent late-phaseCorticosteroids (hydrocortisone 100-300 mg) prevent late-phase
symptoms in severely affected patients.symptoms in severely affected patients.
45. Obstructive shockObstructive shock
Tension pneumothoraxTension pneumothorax
Pericardial disease (temponade, constrictivePericardial disease (temponade, constrictive
pericarditis)pericarditis)
Disease of pulmonary vasculature (massiveDisease of pulmonary vasculature (massive
pulmonary emboli, pulmonary hypertension)pulmonary emboli, pulmonary hypertension)
Cardiac tumor (atrial myxoma)Cardiac tumor (atrial myxoma)
Left atrial mural thrombusLeft atrial mural thrombus
Obstuctive valvular disease (aortic or mitralObstuctive valvular disease (aortic or mitral
stenosis)stenosis)
These are medical emergencies requiring prompt diagnosis & treatmentThese are medical emergencies requiring prompt diagnosis & treatment