This document provides information on arterial blood gas (ABG) interpretation for medical professionals and trainees. It discusses the indications, equipment, and procedures for collecting an ABG sample. Key steps in the collection process include preparing the patient, selecting an appropriate artery site, and applying pressure after puncture. The document then covers interpreting ABG results through a stepwise approach considering pH, acid-base balance, compensation, oxygenation status, and identifying simple vs mixed disorders. Common abnormal values and their implications are presented. Examples of interpreted ABG reports are provided to demonstrate the evaluation process.
one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance
Surfactant replacement therapy : RDS & beyondDr-Hasen Mia
This presentation is about Surfactant, its use in Respiratory Distress Syndrome & some other conditions of surfactant deficiency due to inactivation like meconium aspiration syndrome & others
one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance
Surfactant replacement therapy : RDS & beyondDr-Hasen Mia
This presentation is about Surfactant, its use in Respiratory Distress Syndrome & some other conditions of surfactant deficiency due to inactivation like meconium aspiration syndrome & others
ABG analysis is the measurement of the dissolved oxygen and carbon dioxide in the arterial blood to reveal the acid base balance and how well the oxygen is being carried to the body.
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.
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
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
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.
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Maxilla, Mandible & Hyoid Bone & Clinical Correlations by Dr. RIG.pptx
ABG INTERPRETATION.pptx
1. Dr Venkata Sai kumar
P.G.-J.R.2
Dept. of Pediatrics
Hind Institute of Medical
Sciences, BBK
ABG INTERPRETATION
Dr PRAGATI SISODIA
ASSISTANT PROFESSOR
Dept. of Pediatrics
Hind Institute of Medical
Sciences, BBK
4. Indication
Any sick child
✓ABGA plays an important role in critically ill children with respiratory
distress.
✓Reveals oxygenation status,
✓Adequacy of ventilation and acid-base balance.
✓Significant role in documenting and monitoring respiratory failure,
especially during ventilator and oxygen therapy.
• IT helps in making diagnosis , assessing severity and titrating the
treatment
5. EQUIPMENT
Blood gas kit
• 1ml/2ml syringe
• 23-26 gauge needle
• Stopper or cap
• Alcohol swab
• Disposible gloves
• Plastic bag& crushed ice
• Lidocaine(optional)
• Vial of heparin(1:1000)
• Bar code or label
6. PREPARATORY PHASE:
• Record patient inspired oxygen concentration
• Check patient temperature
• Explain the procedure to the patient
• Provide privacy for client
• If not using heparinised syringe,heparanize the needle
• Perform allen’s test
• Wait at least 20 minutes before drawing blood for ABG after
initiating,changing,or discontinuing oxygen therapy,or
settings of mechanical ventilation,after suctioning the
patient or after extubation
7. ALLEN’S TEST
• It is a test done to determine that collateral circulation is present
from the ulnar artery in case thrombosis occur in the radial
8. Sites for obtaining ABG
• Radial artery(most common)
• Brachial artery
• Femoral artery
Radial is the most preferable site used because:
• It is easy to access
• It is not a deep artery which facilitate
palpation,stabilization and puncturing
• The artery has a collateral blood circulation
10. PERFORMANCE PHASE
• Wash hands
• Put on gloves
• Palpate the artery for maximum pulsation
• If radial,perform Allen’s test
• Place a small towel roll under the patient wrist
• Instruct the patient to breath normally durning the test and warn him that
he may feel brief cramping or throbbing pain at the puncture site
• Clean with alcohol swab in circular motion
• Skin and subcutaneous tissue may be infiltrated with local anesthetic agent
if needed
11. • Insert needle at 45 radial, 60 brachial and 90
femoral
• Withdraw the needle and apply digital pressure
• Check bubbles in syringe
• Place the capped syringe in the container of ice
immediately
• Maintain firm pressure on the puncture site for 5
minutes, if patient has coagulation abnormalities
apply pressure for 10-15 minutes
12. Follow up phase:
• Send labelled,iced specimen to the lab
immediately
• Palpate the pulse distal to the puncture site
• Assess for cold hands,numbness,tingling or
discoloration
• Documentation include: results of Allen’s test, time
the sample was drawn,temperature,puncture
site,time pressure was applied and if O2 therapy is
there
• Make sure its noted on the slip whether the
patient is breathing room air or oxygen. If
oxygen,document the number of litres. If the
patient is receiving mechanical ventilation,FIO2
should be documented
13. Errors in ABG
Excessive heparin
•Dilution Effect on Results decrease in HCO3 - & PaCO2
•Only .05 ml Heparin required for 1ml blood
•So syringe be emptied of heparin after flushing or
only dead space volume is sufficient or dry heparin
should be used
14. AIR BUBBLES
1. PO2 150 mmHg & PCO2 0mm Hg in air bubble(R.A)
2. Mixing with sample,lead to increase PaO2 & decrease in PaCO2
To avoid air bubble,sample drawn very slowly and preferabily in glass
syringe
Steady State:
Sampling should be done during steady state after change in oxygen
therapy or ventilator parameter
Steady state is achieved usually within 3-10 minutes
15. Dilution of blood sample with IV fluids
• Dilution of blood sample with IV fluid will typically lower the PaCO2
and increase the basedeficit without affecting the pH
• This is probably because of the diffusion of CO2 from blood onto the
IV fluid,which contains no CO2.
• Because of the buffering capacityof the blood,the pH changes
little,despite the decrease in PaCO2,giving the appearance of a
combined metabolic acidosis and respiratory alkalosis.
• Dilution of a blood gas sample with a liquid emulsion does not appear
to have any affect on the blood gas measurements. Dry heparin also
does not affect blood gas results.
24. Approach to ABG
• ABG should never be interpreted alone
• Previous blood gases
• Patient clinical status
• X-ray
• Other investigations e.g. Sepsis screening
• You have to treat the patient not the blood gas go with the clinical
picture
30. COMPENSATION
Respiratory compensation
• Respiratory compensation
• Starts within minutes
• complete within 12-24 days
Metabolic compensation
• Starts within Hours
• complete within 2-5 days
• renal base excretion faster
31.
32. Compensation by Respiratory Response to
Metabolic Acidosis
✓Predicted Change in PCO2 = (1.5 x HCO3 + 8)± 2
✓If patient’s PCO2 is roughly this value, his or her response is
appropriate
✓If patient’s PCO2 is higher than this value, they are failing to
compensate adequately
Metabolic Alkalosis
✓Every 10 mmHCO3 increase PaCO2 7
33. In respiratory acidosis, for every 10mm increase in
PaCO2 , HCO3 is increased by 1 in acute condition
and by 3.5 in chronic condition
In respiratory alkalosis, for every 10mmHg
decrease in PaCO2 , HCO3 is decreased by 2 in
acute and by 4 in chronic condition
Compensation by Metabolic Response to
37. Oxygenation Status
o Depends upon age & inspired oxygen concentration (FiO2)
o Normal value of PaO2 is 80-100 mm of Hg in children and adults
o Newborn it ranges from 40-70 mm of Hg
o On oxygen therapy the value of PaO2 will high (PaO2 = FiO2 × 5)
o Oxygen supplementation should below 60% to avoid toxicity
o Anemic patient may have normal PaO2 and SaO2 but final delivery of
O2 to the tissues
will be compromised
o Generally oxygen saturation measured by pulse oximetry (SpO2)
lower than arterial oxygen saturation (SaO2) measured directly by
blood gas analysis.
39. Simple or Mixed Disorder
• In simple acid base disorder, both PaCO2 and HCO3– change in the
same direction
• If they do not follow this trend, the possibility of mixed disorder is
likely
• The expected compensation for simple acid base disorder is
predetermined and
• if they deviate from the norms there is the possibility of mixed
disorder
40. Anion gap
• Difference of unmeasured cations & Anions
• Anion gap(AG)= Na+k-(Cl+HCO3)
• Normal AG Acidosis: RTA, Diarrhoea
• Increase AG acidosis: lactic acidosis,ketoacidosis,uremia
• Normal 8-12
• If >12= high anion gas acidosis
• If <12= non anion gas acidosis
41.
42.
43. Q
• A 6 y male child presented in emergency with c/c of fever and
abnormal body movement
• for 2 days , ABGA was showing following
• pH =7.39
• PaCO2=40.2q
• PO2= 74.5
• HCO3= 22.1
• BE=-0.8
• What is your diagnosis ?
44. Q
• 6-year-old child came with fever for 5 days and rapid breathing since today morning. You
did ABGA which reveals the following results:
what is your interpretation
PaO2: 68.2 mmHg (82.5 – 97.5 mmHg)
pH: 7.30 (7.35 – 7.45)
PaCO2: 63 mmHg (35.2 – 45 mmHg)
HCO3-: 29 (22 – 26 mEq/L)
BE: +4 (-2 to +2)
i. Metabolic Acidosis
ii. Metabolic Acidosis with Respiratory Compensation
iii. Respiratory Acidosis
iv. Respiratory Acidosis with metabolic compensation