ABGs or VBGs interpretation made simple straight forward easy to remember and easy to apply. The presentation is designed to help the residents and junior ER physicians. The second part will discuss the oxygenation and the third part will review the "Stewart Approach" while fourth and last part is meant for the Experts.
ABGs or VBGs interpretation made simple straight forward easy to remember and easy to apply. The presentation is designed to help the residents and junior ER physicians. The second part will discuss the oxygenation and the third part will review the "Stewart Approach" while fourth and last part is meant for the Experts.
Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
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
Acute Kidney Injury-case management and discussion
AKI secondary to sepsis secondary to acute bacterial salphingitis vs TB salphingitis
KDIGO 2012 guidelines
AKI, harrison's 19th edition
Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
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
Acute Kidney Injury-case management and discussion
AKI secondary to sepsis secondary to acute bacterial salphingitis vs TB salphingitis
KDIGO 2012 guidelines
AKI, harrison's 19th edition
lower GI Bleed case presentation and discussion with cause, risk factors, pathology, management and intervention (colonoscopy) and guidelines for the management and screening of colorectal cancer
ANATOMY LAB DISSECTION, LUNGS AND HEART OF HUMAN CADAVER WITH DIFFERENT VIEWS AND LABELING OF EACH STRUCTURE IN EACH SLIDES
FOR MBBS 1ST YEAR, BDS, AND OTHER MEDICAL SCIENCES
Pre diabetes, Diabetes, DM
Public awareness
Public talk show
Glucose impared
Lifestyle management
Healthy life
Normal glucose levels
Impared glucose levels
chronic myeloid leukemia, CML, epidemiology, BCR ABL1 gene, philadelphia chromosome, t(9;22), CML incidence, etiology of CML, pathophysiology of CML, phases of CML, treatment of CML, Allogenic stem cell transplant, TKI therapy for CML, Sokal index for CML,
adult vaccination, types of vaccine, forms of vaccine, active immunity, passive immunity, schedule of vaccination, CDC, contraindications, cost of vaccines
chronic kidney disease, diagnosis, management, prognosis, complications, renal replacement therapy, when to initiate hemodialysis, complication of hemodialysis, mortality and morbility.
mechanism of resistance of antibiotics, ESBL, b lactums, enterobactericae, metallobactums, carbapenemases, types of mechanism of resistance, history of antibiotics and resistance
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.
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!
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
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.
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.
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
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
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
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.
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
2. ABG analysis is an essential component of diagnosing
and managing critically ill patients in the ICU.
A step wise approach to the evaluation of these
disorders helps delineate underlying causes,
compensatory mechanism, and the correct approach
to management.
5. PaO2 and SaO2
PaO2 / FiO2 ratio
e.g. PaO2 :84 mmHg with 0.21 FiO2 [room air]
PaO2 / FiO2 = 84 / 0.21 = 400
Normal = 300 – 500 mmHg
< 300 = acute lung injury [previous definition]
< 200 = ARDS [previous definition]
Berlin definition:
200 – 300 [with PEEP/CPAP > 5] = mild ARDS
< 200 [with PEEP > 5]
= moderate ARDS
<100 [with PEEP > 5]
= severe ARDS
6. Step 1: Acidemic, alkalemic, or normal?
Step 2: Is the primary disturbance respiratory or metabolic?
Step 3: For a primary respiratory disturbance, is it acute or chronic?
Step 4: For a metabolic disturbance, is the respiratory system
compensating OK?
Step 5: For a metabolic acidosis, is there an increased anion gap?
Step 6: For an increased anion gap metabolic acidosis, are there other
derangements?
7. The pH is the –log [H]. So by altering either the PCO2
or the HCO3-, [H] will change, and so will pH.
An acidemia(low pH) can result from either a low
HCO3- or a high CO2
An alkalemia (high pH) can result from either a high
HCO3 or a low CO2
8. If pH and PaCO2 changes in same direction, the
primary disorder is metabolic and if they change in
opposite direction ,the primary disorder is respiratory.
Chemical
change
Primary
disorder
Compensation
pH
Low HCO3-
Metabolic
acidosis
Respiratory
alkalosis
low pH
High HCO3-
Metabolic
alkalosis
Respiratory
acidosis
High pH
High PaCO2
Respiratory
acidosis
Metabolic
alkalosis
Low pH
Low PaCO2
Respiratory
alkalosis
Metabolic
acidosis
High pH
9. Respiratory acidosis is due to a primary rise in CO2
Hypercapnia almost always results from alveolar
hypoventilation due to one of the following causes:
Respiratory center depression
2. Neuromuscular disorder
3. Upper airway obstruction
4. Pulmonary disease
1.
10. A respiratory alkalosis is due to decrease in PaCO2.
It results from hyperventilation leading to decrease in
CO2.
Causes of respiratory alkalosis:
Hypoxemia from any causes
2. Respiratory center stimulation
3. Mechanical hyperventilation
4. Sepsis, pain
1.
11. Normal pH is 7.4
Calculate the change in pH (from 7.4)
A.
in acute respiratory disorder (acidosis / alkalosis)
change in pH = 0.008 X [PaCO2 -40]
expected pH = 7.4 +/-change in pH
B. in chronic respiratory disorder (acidosis/alkalosis)
change in pH = 0.003 X [PaCO2 -40 ]
expected pH = 7.4 +/- change in pH
Compare the pH on ABG
if pH on ABG is close to A, it is acute disorder
if pH on ABG is close to B, it is chronic disorder
12. M/60 yrs, k/c/o C.O.P.D. admitted with U.T.I.
ABG: 7.26 / 84 / 74 / 37 / 94%
[A]. For Acute change in pH;
change in pH = 0.008 X [84 – 40 ] =0.008 X [44] =0.35
Expected pH = 7.4 – 0.35 = 7.05
[B]. For chronic change in pH’
Change in pH = 0.003 X [84 – 40 ] = 0.003 X [44] = 0.13
Expected pH =7.4 -0.13 = 7.27
So B is near to the patient’s ABG which is 7.26; so primary disorder
is chronic respiratory acidosis.
13. Primary
disorder
Initial Compens Compensa
chemic a-tory
al
response tory
change
mechanis
s
m
Respiratory
acidosis
Expected level of compensation
↑PCO2 ↑HCO3-
Acute
Bufferingrule of 1
↑[HCO3-] = 1 mEq/L for every
10 mmHg delta PCO2
Chronic
Generation
of new
HCO3 –
rule of 3
[HCO-] = 3 mEq/L for every
10mmHg delta PCO2
18. Metabolic alkalosis reflects an increase in plasma
[HCO3-]
It can be classified into saline responsive or
nonresponsive.
More than 20 mEq/L urinary chloride is saline
unresponsive and less than 20 mEq/L is saline
responsive.
19. Causes of Urine CL > 20 mEq/L
Causes of Urine CL < 20 mEq/L
Mineralocorticoid excess
Vomiting, nasogastric suctioning
K + and Mg ++ deficiency
chloride-wasting diarrhea
Liddle’s syndrome
Villous adenoma of colon
Barter’s syndrome
Posthypercapnia
Hypercalcemia with secondary
hyperparathyroidism
Poorly reabsorbed anions like
carbenicillin
Milk – alkali syndrome
Diuretic therapy
20. Calculate AG in case of metabolic acidosis
High denotes raised AG metabolic acidosis, and
normal or narrow denotes non-AG acidosis.
21. It is used to determine if a metabolic acidosis is due to
an accumulation of non- volatile acids [e.g. lactic
acidosis] or a net loss of bicarbonate [e.g. diarrhea]
Na + UC = [ Cl + HCO3 ] + UA
UA – UC [ Anion gap] = Na –[ Cl + HCO3- ]
AG= Na –[Cl + HCO3]; normal AG is 12+/-2 mEq/L
22. Unmeasured Anions
Unmeasured Cation
Albumin: 15 mEq/L
Calcium: 5 mEq/L
Organic Acids: 5 mEq/L
Potassium: 4.5 mEq/L
Phosphate: 2 mEq/L
Magnesium: 1.5 mEq/L
Sulfate: 1 mEq/L
Total UA: 23 mEq/L
Total UC: 11 mEq/L
Anion AG = UA – UC = 12 mEq/L
Adjusted AG = calculated AG + 2.5 X [4 – S.albumin gm%]
23. 7.23 / 34 /88 /17 : Metabolic Acidosis
Na : 135 / Cl: 99 / K: 3.5
AG = Na - [ Cl + HCO3-] = 135 – [ 99 + 17] = 19
High AG
26. Check urinary AG in non-AG metabolic acidosis
U Na + U K – U Cl
Normal :
negative
Non-renal loss of bicarbonate [diarrhea] : negative
Renal loss of bicarbonate[ RTA /
H+ excretion]
: positive
27. In less obvious cases, the coexistence of two metabolic
acid-base disorders may be apparent by calculating the
difference between the change in AG [delta AG] and
the change in serum HCO3- [delta HCO3-].
e.g. Diabetic ketoacidosis
This is called the Delta gap or gap –gap.
28. Delta gap = delta AG – delta HCO3 Where delta AG = patient’s AG – 12 mEq/L
Delta HCO3- = 24 mEq/L – patient’s HCO3 Normally the delta gap is zero :
AG acidosis
A positive delta gap of more than 6 mEq/L :
metabolic alkalosis and/or HCO3- retention.
The delta gap of less than 6 mEq/L :
Hypercholremic acidosis and/or HCO3- excretion.
29. 7.23 / 34 /88 /17 : Metabolic Acidosis
Na : 138 / Cl: 99 / K: 3.5
AG = Na - [ Cl + HCO3-] = 138 – [ 99 + 17] = 22
Next step is to calculate the Delta Gap.
Delta AG = patient’s AG -12 = 22 – 12 = 10
Delta HCO3- = 24 – patient’s HCO3- = 24 – 17 = 7
Delta gap = Delta AG- Delta HCO3- = 10 – 7 = 3
Additional metabolic alkalosis is also present with high AG
metabolic acidosis.
30. Step 1: Acidemic, alkalemic, or normal?
Step 2: Is the primary disturbance respiratory or metabolic?
Step 3: For a primary respiratory disturbance, is it acute or chronic?
Step 4: For a metabolic disturbance, is the respiratory system
compensating OK?
Step 5: For a metabolic acidosis, is there an increased anion gap?
Step 6: For an increased anion gap metabolic acidosis, are there other
derangements?
31. 65 years old male with CKD presenting with nausea,
diarrhea and acute respiratory distress
ABG: 7.23/17/235/7 with 50% FiO2 on V.M.
Electrolytes: Na: 123 mEq/L, Cl: 97 mEq/L, S.K 3.5
Renal function: S. Creat: 5.1 mg%, BUN: 119
33. Respiratory / metabolic ?
ABG: 7.23/17/235/7 with 50% FiO2 on V.M.
pH and PaCO2 goes in same direction; so it is
primarily metabolic disorder.
34. ABG: 7.23/17/235/7 with 50% FiO2 on V.M.
Winter’s formula:
Expected PaCO2 = 1.5 X [7] + 8 +/- 2 = 18.5 +/-2
35. ABG: 7.23/17/235/7 with 50% FiO2 on V.M.
Electrolytes: Na: 123 mEq/L, Cl: 97 mEq/L, S.K 3.5
AG = Na – [Cl +HCO3-] = 123 – [97 + 7] = 19
High AG metabolic acidosis
Delta gap = Delta AG – Delta HCO3-
= [19 - 12 ] – [24 – 7 ]
=7–7=0
Non –anion gap metabolic acidosis
36. High AG metabolic acidosis with non-anion metabolic
acidosis
37. High AG metabolic acidosis is due to BUN 119
Non anion metabolic acidosis is due to diarrhea
38. Very sick 56 year old man being evaluated for a
possible double lung transplant
Dyspnoea on minimal exertion
On home oxygen therapy
(nasal prongs, 2 lpm)
Numerous pulmonary medications
ABG: 7.30/65/88/31.1
44. Patient has a long standing pulmonary disease so
bicarbonate is in the compensation.
45. A 44 year old moderately dehydrated man was
admitted with a two day history of acute severe
diarrhea.
ABG: 7.31 / 33 / 88 /16 / 95%
Elect: Na: 136 mEq/L, Cl: 103 mEq/L, K: 2.9 mEq/L
51. Patient lost bicarbonate in diarrhea leading to non
anion gap metabolic acidosis.
52. A 38-year-old woman is 12 weeks pregnant. For the last 10
days she has had worsening nausea and vomiting. When
seen by her physician, she is dehydrated and has shallow
respirations. Arterial blood gas data is as follow
ABG: 7.56/54/110/45
57. Patient has lost lot of gastric juice and hydrochloric
acid in vomit leading to metabolic alkalosis.
58. Step 1: Acidemic, alkalemic, or normal?
Step 2: Is the primary disturbance respiratory or metabolic?
Step 3: For a primary respiratory disturbance, is it acute or chronic?
Step 4: For a metabolic disturbance, is the respiratory system
compensating OK?
Step 5: For a metabolic acidosis, is there an increased anion gap?
Step 6: For an increased anion gap metabolic acidosis, are there other
derangements?