This document provides guidance on preparing for exit exams for a medical degree. It discusses the exam format, which will include 3 papers, with the third being an evidence-based medicine paper. It emphasizes the importance of taking detailed notes from source materials, creating a one-page summary, and structuring answers for exam questions to address topics like diagnosis, prognosis, management, etc. Sample questions and examples are provided. Resources for pathology, figures, tables and a one-page approach to shock are also referenced to aid preparation.
Intro to Hypoxic pulmonary vasoconstriction Arun Shetty
Hypoxic pulmonary vasoconstriction, a seldom heard phenomenon but very effective physiologic property which helps lungs utilise ventilation to the maximum
Intro to Hypoxic pulmonary vasoconstriction Arun Shetty
Hypoxic pulmonary vasoconstriction, a seldom heard phenomenon but very effective physiologic property which helps lungs utilise ventilation to the maximum
Non invasive estimation of pulmonary vascular resistance in patients of pulmo...Arindam Pande
Context : Pulmonary vascular resistance (PVR) is a critical and essential parameter during the
assessment and selection of modality of treatment in patients with congenital heart
disease accompanied by pulmonary arterial hypertension.
Aim : The present study was planned to evaluate non-invasive echocardiographic parameters
to assess pulmonary vascular resistance.
Settings and
Design
: This prospective observational study included 44 patients admitted in the cardiology
and pediatric cardiology ward of our institution for diagnostic or pre-operative catheter
based evaluation of pulmonary arterial pressure and PVR.
Materials and
Methods
: Detailed echocardiographic evaluation was carried out including tricuspid regurgitation
velocity (TRV) and velocity time integral of the right-ventricular outflow tract (VTIRVOT).
These parameters were correlated with catheter-based measurements of PVR.
Results : The TRV/VTIRVOT ratio correlated well with PVR measured at catheterization
(PVRcath) (r = 0.896, 95% confidence interval [CI] 0.816 to 0.9423, P < 0.001). Using
the Bland-Altman analysis, PVR measurements derived from Doppler data showed
satisfactory limits of agreement with catheterization estimated PVR. For a PVR of 6
Wood units (WU), a TRV/VTIRVOT value of 0.14 provided a sensitivity of 96.67% and
a specificity of 92.86% (area under the curve 0.963, 95% confidence interval 0.858 to
0.997) and for PVR of 8 WU a TRV/VTIRVOT value of 0.17 provided a sensitivity of
79.17% and a specificity of 95% (area under the curve 0. 0.923, 95% confidence interval
0.801 to 0.982).
Conclusions : Doppler-derived ratio of TRV/VTIRVOT is a simple, non-invasive index, which can be
used to estimate PVR.
Non invasive estimation of pulmonary vascular resistance in patients of pulmo...Arindam Pande
Context : Pulmonary vascular resistance (PVR) is a critical and essential parameter during the
assessment and selection of modality of treatment in patients with congenital heart
disease accompanied by pulmonary arterial hypertension.
Aim : The present study was planned to evaluate non-invasive echocardiographic parameters
to assess pulmonary vascular resistance.
Settings and
Design
: This prospective observational study included 44 patients admitted in the cardiology
and pediatric cardiology ward of our institution for diagnostic or pre-operative catheter
based evaluation of pulmonary arterial pressure and PVR.
Materials and
Methods
: Detailed echocardiographic evaluation was carried out including tricuspid regurgitation
velocity (TRV) and velocity time integral of the right-ventricular outflow tract (VTIRVOT).
These parameters were correlated with catheter-based measurements of PVR.
Results : The TRV/VTIRVOT ratio correlated well with PVR measured at catheterization
(PVRcath) (r = 0.896, 95% confidence interval [CI] 0.816 to 0.9423, P < 0.001). Using
the Bland-Altman analysis, PVR measurements derived from Doppler data showed
satisfactory limits of agreement with catheterization estimated PVR. For a PVR of 6
Wood units (WU), a TRV/VTIRVOT value of 0.14 provided a sensitivity of 96.67% and
a specificity of 92.86% (area under the curve 0.963, 95% confidence interval 0.858 to
0.997) and for PVR of 8 WU a TRV/VTIRVOT value of 0.17 provided a sensitivity of
79.17% and a specificity of 95% (area under the curve 0. 0.923, 95% confidence interval
0.801 to 0.982).
Conclusions : Doppler-derived ratio of TRV/VTIRVOT is a simple, non-invasive index, which can be
used to estimate PVR.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
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
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
10. IF YOU HATE WRITING NOTES
( YOU SHOULDN’T)
• TAKE A PRINT OF 1 ARTICLE
• ADD ALL THE POINTS FROM DIFFERENT SOURCES TO THIS ARTICLE
• AT A LATER STAGE YOU NEED TO READ THIS ONE ARTICLE ONLY
14. EVERY Q ON MANAGEMENT
• DIAGNOSIS
• PROGNOSIS
• ACUTE MANAGEMENT
• GENERAL MANAGEMENT
• DEFINITIVE MANAGEMENT
• LONG TERM MANAGEMENT
• REHABILITATION
• ANTICOAGULATION
15. EXAMPLES OF HOW TO WRITE ANSWERS
Q. MANAGEMENT OF ACUTE PE ?
16.
17.
18. Q. INDICATION FOR ALBUMIN WITH EVIDENCE
INDICATION
• CLD WITH ASCITES
• HRS
EVIDENCE
• ANSWER TRIAL –
• 40 G OF ALBUMIN TWICE A WEEK FOR THE INITIAL 2 WEEKS AND
THEN 40 G ONCE A WEEK FOR 18 MONTHS.
• MORTALITY BENEFIT
• CONFIRM TRIAL
• TERLIPRESSIN WITH ALBUMIN, IS ASSOCIATED WITH HIGHER
LIKELIHOOD OF REVERSAL OF HRS AND 10-DAY SURVIVAL
WITHOUT RRT
ETC
22. by Nick Mark MD
APPROACH TO UNDIFFERENTIATED SHOCK onepageric
u.com
@nickmma
rk
Link to the
most current
version →
ONE
Undifferentiated SHOCK
CARDIOGENIC OBSTRUCTIVE DISTRIBUTIVE HYPOVOLEMIC
PUMP PROBLEM
PIPES PROBLEM TANK PROBLEM
• RATE/RHYTHM (bradycardia, VF, etc)
• RV FAILURE (PE, PHTN)
• LV FAILURE (MI, myocarditis, etc)
• VALVES (wide open MR, cordae tendenae
rupture, etc)
• TOXINS (CCB, βB, BRASH syndrome, etc)
• TRAUMA (myocardial contusion)
• TENSION PNEUMOTHORAX
• CARDIAC TAMPONADE
• PULMONARY EMBOLISM
• OUTFLOW OBSTRUCTION (HOCM,
critical AS)
• DYNAMIC HYPERINFLATION (auto-
PEEP)
• SEPSIS (may develop low CO later)
• ANAPHYLAXIS
• INFLAMMATORY (SIRS, pancreatitis,
post-cardiac arrest, amniotic or fat
embolism, cytokine release syndrome)
• NEUROGENIC (SCI, severe TBI, effect of
neuraxial anesthesia)
• LIVER FAILURE
• ENDOCRINE (adrenal insufficiency,
thyrotoxicosis)
• MEDICATIONS (anesthesia, sedation)
• HEMORRHAGE (trauma, surgical, GIB)
• SKIN LOSSES (burns, heat stroke, etc)
• GI LOSSES (diarrhea, vomiting, drainage)
• THIRD-SPACING VOLUME LOSS
(pancreatitis, low albumin, trauma)
• RENAL LOSSES (salt-wasting, hypoaldo,
osmotic diuresis, diuretics)
• LOW PO INTAKE
EXAM
&
POCUS
&
H
EMODYNAMICS
v1.0
(2021-05-11)
CC
BY-SA
3.0
ETIOLOGY
· Shock occurs when there is inadequate blood flow (CO) & oxygen delivery (DO2) to meet
demands. Manifestations can be protean and may not initially include hypotension (cryptic
shock). Identifying the etiology of undifferentiated shock is essential to determine treatment.
· Shock can be broken into 4 categories: cardiogenic, obstructive, distributive, hypovolemic
· Multiple causes may be present (e.g. sepsis in a patient with decompensated heart failure)
and some etiologies may cause mixed shock:
· Endocrine (adrenal insuf., myxedma, thyrotoxicosis)
· Metabolic (hypothermia severe acidosis)
HD ↑CVP, ↑PCWP, ↓CO, ↑SVR ↑CVP, ↑PCWP, ↓CO, ↑SVR var CVP, var PCWP, var CO, ↓SVR ↓CVP, ↓PCWP, ↑CO, ↑SVR
Heart
± Reduced contractility ± RV dilation
± Wall motion abnormalities
± Valvulopathy
Reduced contractility
RV dilation (PE) ± septal D sign (p/v overload)
Pericardial effusion, RA collapse (tamponade)
Hyperdynamic
(hypodynamic in late sepsis)
Hyperdynamic
IVC Plethoric IVC, reversal of flow in HV Plethoric IVC, reversal of flow in HV Variable IVC Small/collapsing IVC
Lungs B-line pattern + pleural effusions Lack of lung sliding ± lung point (PTX) A line pattern A line pattern
Other Pleural effusions (LV failure) DVT or clot in transit (PE) Evidence of infxn (cholecystitis, endocarditis,
etc), cirrhosis,
Blood or fluid in abdomen (FAST), Ectopic
pregnancy, Aortic dissection,
Skin Usually cool, Delayed cap refill Usually cool, Delayed cap refill Warm, flushed, Brisk cap refill Usually cool, Delayed cap refill
Neck Increased JVP Increased JVP Variable Flat neck veins
Other Weak pulses (narrow pulse pressure)
Weak pulses (narrow pulse pressure)
Lung and heart sounds are unreliable
indicators of tamponade or PTX.
Bounding pulses (wide pulse pressure)
Weak pulses (narrow pulse pressure)
Evidence of blood (pallor) or volume loss
(axillary dryness)
𝑺𝑽𝑹 =
(𝑴𝑨𝑷 − 𝑪𝑽𝑷)
𝑪𝑶
× 𝟖𝟎
𝑵𝒐𝒓𝒎𝒂𝒍 𝑺𝑽𝑹 = 𝟖𝟎𝟎 − 𝟏𝟔𝟎𝟎 dyn/cm/sec-5
= 𝟏𝟎 − 𝟐𝟎 Wood units
↓CO ↓ Preload
↓SVR
𝑴𝑨𝑷 = 𝑪𝑶 × 𝑺𝑽𝑹
Hypotension (not required)
Organ dysfunction (AKI, shock liver, etc)
Altered mental status
Lactic acidosis
Low urine output
CALCULATING SVR:
SVR can be useful to understand etiology. You
can either measure CO invasively (e.g. PAC) or
estimate using POCUS (e.g. LVOT VTI)
RAP
Venous
Return
CARDIOGENIC/OBSTRUCTIVE
with low CO, RA filling pressures
rise to (partially) compensate
Cardiac
Output
RAP
Venous
Return
HYPOVOLEMIC
with low preload, venoconstriction
increased filling pressure compensates
Cardiac
Output
PHYSIOLOGIC RESPONSES TO SHOCK USING GUYTON CURVES:
RAP
Venous
Return
DISTRIBUTIVE
vasodilation decreases filling,
hyperdynamic CO compensates
Cardiac
Output
Preload Contractility
SV HR
CO SVR
MAP
Afterload
MAP DETERMINANTS:
RAP
Venous
Return
Cardiac
Output
Normally cardiac output (CO)
determined by venous return &
contractility
(See Guyton Curves in Shock OnePager for more)
(see
RUSH
exam
for
more
about
POCUS
in
Shock)
Increased
contractility
Venoconstriction
with exercise
initial state
23. by Nick Mark MD
HYPOXIA & HYPOXEMIA onepageric
u.com
@nickmma
rk
Link to the
most current
version →
ONE
Hypoxia – insufficient oxygen delivered to tissues to meet demands
Hypoxemia – low oxygen in the blood (most common type of hypoxia)
PIO2 – atmospheric oxygen (how much O2 is inspired)
PAO2 – alveolar oxygen (how much O2 reaches the alveoli)
PaO2 – oxygen dissolved in arterial blood (measured on ABG)
SaO2 – percent saturation of hemoglobin in arterial blood
CaO2 – oxygen content of art. blood (dissolved & Hb bound)
DEFINITIONS:
𝐃𝑶𝟐 = 𝑯𝑹 × 𝑺𝑽 × 𝟏. 𝟑𝟒 × 𝑯𝒃 × 𝑺𝒂𝑶𝟐 + (𝑷𝒂𝑶𝟐 × 𝟎. 𝟎𝟎𝟑)
HYPOXEMIC HYPOXIA
Insufficient oxygen in the blood
(the most common type of hypoxia)
Low PaO2
CYTOPATHIC HYPOXIA
Cells cannot use oxygen
(e.g. cyanide toxicity, maybe sepsis)
High PaO2, High SvO2
O2 bound to hemoglobin O2 dissolved in blood
Tissue hypoxia occurs when DELIVERY OF OXYGEN (DO2) is inadequate to meet
metabolic demands. DO2 depends on CARDIAC OUTPUT (CO) & the
OXYGEN CONTENT OF BLOOD (CaO2)
CO
LOW INSPIRED OXYGEN (PIO2) ALVEOLAR HYPOVENTILATION V/Q MISMATCH SHUNT DIFFUSION LIMITATION
LOW MIXED VENOUS O2 (SVO2)
𝑷𝑨𝑶𝟐 = 𝑭𝒊𝑶𝟐 × 𝑷𝒂𝒕𝒎 − 𝑷𝑯𝟐𝑶 −
𝑷𝒂𝑪𝑶𝟐
𝑸
The Aa DIFFERENCE is the ALVEOLAR OXYGEN TENSION (PAO2)
minus the ARTERIAL OXYGEN TENSION (PaO2), reflecting
the efficiency of oxygen exchange. It is used to
identify the etiology of hypoxemic hypoxia:
pulmonary causes have ↑ Aa difference whereas
extra-pulmonary etiologies (↓ PiO2, ↓SvO2, &
alveolar hypoventilation) have nl Aa difference.
Fewer oxygen molecules enter the
lungs with respiration (low PAO2)
· Normal Aa difference
· PaO2 normalizes with supplemental
oxygen
· Causes: low atmospheric pressure
(e.g. high altitude), or low partial
pressure of oxygen (FiO2 < 0.21 e.g.
confined space, low O2 gas mixtures)
Fewer O2 molecules reach the alveoli
due to decreased ventilation (low
PAO2).
· Normal Aa difference
· PaO2 normalizes with supplm. O2
· Increased PaCO2
· Causes: decreased respiratory drive
(opioids, brainstem stroke, OHVS),
neuromuscular weakness (GBS, ALS),
chest wall problems (kyphoscoliosis,
flail chest) or airflow obstruction
(COPD, asthma)
Imbalance between regional lung
ventilation and perfusion (low V/Q).
Most common cause of hypoxemia.
· Increased Aa difference
· PaO2 normalizes with suppl. O2
· Causes: obstructive lung diseases
(COPD), pulmonary vascular disease
(PE), alveolar filling processes
(pneumonia, pulmonary edema),
interstitial disease & atelectasis
Blood passes from the right side of
the heart to the left side without
being oxygenated.
· Increased Aa difference
· PaO2 does NOT normalize with
supplemental oxygen
· Causes: anatomical(ASD, VSD,
pulm AVMs) & physiological shunts
(atelectasis, pneumonia, ARDS)
where blood bypasses alveoli
without effective gas exchange
Impaired O2 diffusion from alveoli to
RBC, causing hypoxemia particularly
in with increased cardiac outpu.
· Increased Aa difference
· PaO2 normalizes with supplm. O2
· Causes: pulmonary fibrosis, edema,
& inflammation that impair gas
exchange in the alveoli
𝑨𝒂 𝒅𝒊𝒇𝒇𝒆𝒓𝒆𝒏𝒄𝒆 = 𝑷𝑨𝑶𝟐 − 𝑷𝒂𝑶𝟐
Venous blood returning to the lungs
(SvO2) has very low O2 due to
increased extraction.
· Normal Aa difference
· PaO2 normalizes with
supplemental oxygen
Causes: severe anemia (low CaO2
rarely a problem unless Hb <5), low
cardiac output, & extremely high
oxygen consumption
OXYGEN DELIVERY:
Aa DIFFERENCE (aka Aa GRADIENT):
Atmospheric pressure
(760 mmHg @ sea level, 630 mmHg @
1500m, 530 mmHg @ 3000m)
H2O vapor pressure
(47 mmHg in the lungs)
Respiratory
Quotient
(normally ~0.8)
𝑵𝒐𝒓𝒎𝒂𝒍 𝑨𝒂 𝒅𝒊𝒇𝒇𝒆𝒓𝒆𝒏𝒄𝒆 =
𝑨𝒈𝒆 𝒚𝒓𝒔 + 𝟏𝟎
𝟒
v1.0
(2020-12-06)
CC
BY-SA
3.0
Alveolar CO2 tension
(assumed to be equal to
arterial CO2)
SvO2 = 50%
CvO2 = 10
SaO2 = 85%
CaO2 = 17
SvO2 = 70%
CvO2 = 15
SaO2 = 98%
CaO2 = 20
PaO2 = 95
SvO2 = 70%
CvO2 = 15
SaO2 = 95%
CaO2 = 19
PAO2
=100
↓PAO2 ↓↓PAO2
= 0
SvO2 = 70%
CvO2 = 15
SaO2 = 85%
CaO2 = 17
Borderline
normoxemia at
rest
With increased blood
flow frank hypoxemia
ensues
unable to fully
oxygenate the
extremely
deoxygenated
venous blood
Low PAO2 due to ↓
ventilation relative to
perfusion in one area
(PAO2 & PaO2 will
normalize with
supplemental O2)
MIXED
VENOUS
BLOOD
ARTERIAL
BLOOD
No O2 exchange
occurs and blood is
not oxygenated
(PaO2 will not fully
normalize with
supplemental O2)
↓PAO2 ↓PAO2
NL PAO2
PIO2
=140
ISCHEMIC HYPOXIA
Insufficient blood flow to tissues,
also called stagnant hypoxia
(e.g low cardiac output)
Low SvO2 Low PaO2
ANEMIC HYPOXIA
Insufficient O2 carrying capacity
(e.g. severe blood loss) or abnormal
hemoglobin (e.g. COHb, MetHb)
Low CaO2 Low SvO2 Low PaO2
Low PAO2 due to
globally reduced
ventilation
(PAO2 & PaO2 will
normalize with
supplemental O2) HB
SATURATION
SaO2
DISSOLVED O2 PaO2
100%
80%
60%
40%
20%
20 40 60 80 100
O
2
CONTENT
CaO2
20 13
16 11
12 8
8 5
4 3
@Hb
=
15
@Hb
=
10
26. AREAS WE
NEGLECT BUT
SURE
QUESTIONS
• STATISTICS
• MEDICAL ETHICS
• COMMUNICATION
• EMPATHY, HUMANISATION
• QUALITY PARAMETERS
• INCIDENT REPORTING
• FIRE IN ICU
• EOLC AND WLST- LEGAL STATUS
27. THE FINAL PART
• REVISE , REVISE, REVISE
READING WITH OUT WRITING NOTES = NOT
READING
READING AND WRITING NOTES WITHOUT
REVISING IT AGAIN AND AGAIN = NOT
READING AT ALL
28. WRITING THE EXAM
• 10 QUESTIONS – 180 MIN
• EACH QUESTION SHOULDNT EXCEED 5 PAGES
• 50 PAGE BOOKLET YOU WILL GET . NO EXTRA BOOKLETS
• INITIAL TIME MARK THE QUESTION NUMBER IN THE SPECIFIC PAGE
• Q2 ON 6TH PAGE , Q3 ON 11TH PAGE ETC
• TRY TO COMPLETE ANSWER IN 15 MINS … DIFFICULT THOUGH
32. WHAT ALL TO READ ?
• CASES
• ALL THE NOTES YOU HAVE WRITTEN FOR
THEORY
• CLINICAL EXAMINATION
• ALL THE TOPICS COVERED IN DEPT
PRESENTATIONS
• ACLS BLS ATLS
• ECG
• VENTILATOR WAVEFORMS
• STATISTICS
• AGAIN COMMUNICATION, ETHICS , INCIDENT
ETC
33. IN SHORT
• READ EVERYTHING IN CRITICAL CARE
• WELL STRUCTURED EXAM
• IN ONE DAY EXAMINERS WILL ASSESS
ALL THE NECESSARY
COMPETENCIES IN CRITICAL CARE
• BROAD QUESTIONS BUT NOT DEEP
• IF YOU FUMBLE THEY WILL GO DEEP
34. LONG CASE
• MULTI SYSTEM INVOLVEMENT
• 30 MIN FOR CASE TAKING – IS IT
ENOUGH ?
• 30 MIN DISCUSSION
35. CASE TAKING
• LEARN A FORMAT – CRITICAL CARE FORMAT
• GENERALLY EXAMINERS DIDNT FOCUS ON THE FORMAT
• NOT MUCH FOCUS ON HISTORY OR NEGATIVE HISTORY
• JUST PATIENT CAME WITH FEVER, MYALGIA 5 DAYS , DEVELOPED
BREATHLESSNESS -> INTUBATED -> DEVELOPED AKI UNDERWENT CRRT
INITIAL LABS SHOWED THROMBOCYTOPENIA . NOW DAY 5
• THEY WILL START WITH DDS AND GO ON
• SOME DIDN’T BOTHER ABOUT EXAMINATION
• SOME DID AND EVEN ASKED TO DEMONSTRATE SUPERFICIAL & DEEP
PALPATION OF ABDOMEN
36. EXAMINATION
• BUT DON’T FORGET TO NOTE DOWN THE FOLLOWING
• EXAMINATION FINDINGS
• TUBES, LINES , DRAINS, CATHETER – DAY , SIZE ETC // NG OR NJ OR ORAL
• WHAT ALL INFUSIONS GOING
• WHAT ALL DRUGS GOING
• IF CRRT THE PRESCRIPTION
• MONITORS & ALARM SETTINGS
• VENTILATOR & ALARM SETTINGS
• CUFF PRESSURE , ALINE WHEN ZEROED ETC
• FASTHUG BID
• LABS & IMAGES
37. USG DURING
EXAMINATION
• IF YOU ASK THEY WILL GIVE
• IF TIME PERMITS YOU CAN DO
• EXAMINERS NOT CONCERNED AS ANOTHER STATION ON
USG IS THERE IN AFTERNOON
• BUT SOME MAY WANT IT TO BE DONE. SO BETTER ASK FOR
IT. IF THEY SAY NO NEED THEN ITS OK
• 30 MIN MEANS 30 MINS
• YOU CAN SCRIBBLE DOWN IN THE ANS SHEET
• DON’T EXPECT TO WRITE IN A DETAILED MANNER
38. THINGS BETTER SAID THAN DONE
BUT IF DONE SUCCESS SURE
• BE CONFIDENT
• PRESENCE OF MIND – V IMP
• THINK LIKE A CONSULTANT AND WHAT YOU
REGULARLY DO AT BED SIDE
• NEVER THINK LIKE AN EXAMINEE
• EVEN IF YOU GET A HIT DON’T BOTHER
• QS ARE GENERALLY PRACTICAL ONES
• THEY EXPECT PRACTICAL ANSWERS RATHER THAN
BOOKISH ONES
39. SHORT CASE
• WILL BE A SYSTEM
• JUST FOCUS ON THAT ONLY
• NO NEED TO LOOK AT OTHER ASPECTS OF THE CASE
• IT CAN BE
• TRACHEOSTOMY
• NUTRITION
• SHOCK
• HFNC/NIV
• CRRT
• A LINE
40. NOT TO MISS POINTS
EXAMINERS MIGHT BE KEENLY OBSERVING
• YOU ARE GREETING PATIENTS OR NOT
• INTRODUCE YOURSELVES TO PATIENT & NURSE
• OBTAINING CONSENT BEFORE EXAMINATION FROM PATIENT & STAFF
• EVEN THE SEDATED PATIENT AS WELL WHILE DOING USG AND ECHO IN AFTERNOON STATIONS
• EVEN IN BRAIN DEAD YOU HAVE TO DO THIS
• HAND HYGIENE
• ALWAYS ASK FOR DISPOSABLE GOWNS AND GLOVES BEFORE TOUCHING PATIENT
41. MORE THAN WHAT YOU READ,
WHAT YOU HAVE DISCUSSED
REPEATEDLY WILL COME TO YOUR
MIND
43. VENTILATON
• DIFFERENT MANUEVERS
• WAVE FORMS NOT ONLY THE SUPERFICIAL ONES LIKE PV LOOPS
• IN DEPTH LEARNING OF WAVEFORMS IN DIFFERENT MODES ,
ASYNCHRONIES
• IDENTIFICATION OF MODE FROM WAVEFORM
• TROUBLE SHOOTING
• NEEDS DEEP READING , RE READING AND EXTENSIVE PRACTICE
• READING ALONE WONT HELP TO MASTER IT
• ESSENTIAL FOR DRNB & EDIC 2
46. IMAGING & INVESTIGATIONS
• CT BRAIN ABDOMEN CHEST
• MRI UNLIKELY
• USG IMAGES
• CXR
• BLOOD CULTURE REPORTS
• CAN BE ASKED ABOUT MANAGEMENT OF THE
ISSUE
• PANCREATITIS IS A FAVOURITE FOR EDIC &
DRNB
48. ACLS, HEMODYNAMICS
• PERFORM BLS, ACLS
• CAN GO INTO MX OF STEMI , STROKE ,
ICD , ATLS ,POST CARDIAC ARREST CARE
• IABP WAVEFORMS , PICCO IMAGES
49. ECG
• ANOTHER AREA WHICH NEEDS FOCUS
• IN DEPTH KNOWLEDGE BETTER
• TO MASTER IT YOU HAVE TO PRACTICE IT
• NO OTHER WAY
• ESSENTIAL FOR EDIC 2 & DRNB
• HAVE TO GO BEYOND ST ELEVATION , AF
53. USG ECHO
• SOME CENTRES ASKED TO DEMONSTRATE ON HEALTHY
VOLUNTEERS
• SOME CENTRES KEPT VIDEOS & IMAGES ONLY
• BASIC VIEWS , LUNG SIGNS , VTI
• GENERALLY THEY ARE NOT MUCH BOTHERED WHETHER
WINDOW IS GOOD OR NOT
• DON’T FORGET TO USE GLOVES, INTRODUCE , OBTAIN
CONSENT & WIPE OFF GEL
55. THESIS
• COMMENT ON WHAT YOU DID
• THEY WILL ASK LIMITATIONS
• THEY WILL FIND SOME EXTRA LIMITATIONS
• QS ON STATISTICS TERMS USED IN THESIS
• OR ANY TECHNIQUE USED IN THE LITERATURE
• WILL NOT ASK HOW YOU CALCULATED SAMPLE ETC
56. CRITICAL APPRAISAL
• 1 ARTICLE WILL BE GIVEN AFTER MORNING SESSION
• DURING THE BREAK ANALYSE THAT
• VERY DIFFICULT AFTER A TRAUMATIC MORNING SESSION
• JUST SUPERFICIAL POINTS YOU CAN TELL
• NOT EXPECTED TO ANALYSE AS IN BOTTOM LINE
57. COMMUNICATION ,
LEGAL , ETHICS
• BREAKING BAD
• VIOLENT BYSTANDER
• MEDICOLEGAL ASPECTS
• BYSTANDER NOT WILLING TO DISCONNECT AFTER
POSITIVE APNEA
• SINGLE BED AVAILABLE – 20 YR TBI WITH GCS 3 &
DILATED PUPILS VS 80 YR HEALTHY WITH CAP ON
VENTILATOR WHOM WILL YOU PREFER AND
WHICH ASPECT OF ETHICS
58. AUDIT,
PATIENT
SAFETY,
QUALITY
SETTING UP AN ICU – QUALITY PARAMETERS, INFRASTRUCTURE
QUALITY INDICATORS IN ICU
FIRE IN ICU
HOW TO DO AN AUDIT
INCIDENT REPORTING
1 AMP MORPHINE MISSING – FOUND EMPTY AMP IN BATHROOM PROCEED
MISMATCHED BLOOD TRANSFUSION -> PROCEED
59. RESOURCES FOR CASES
• DEPARTMENTAL CASE DISCUSSION – READ & MAKE NOTES
• 2 FOAMED GROUPS IN YOUTUBE
60. RESOURCES – ECG
EXCELLENT BOOK FOR BASICS & CONCEPTS
VERY EASY TO UNDERSTAND
FOR PRACTICE
MANY ONLINE
RESOURCES ARE
THERE
ALL BOOKS FOR
EDIC2 ALSO USEFUL
62. SUGGESTIONS
FOCUS ON VENTILATOR , ECG AND ETHICS , QUALITY , COMMUNICATION
DON’T KEEP THESE FRINGE TOPICS FOR LAST - YOU WONT GET TIME AS LOT OF CASES AND CORE TOPICS WILL BE THERE TO READ
BE FAMILIAR WITH EXAMINATION OF SYSTEMS
TIME MANAGEMENT IN THEORY
DON’T FORGET FIGURES , TABLES , FLOW CHARTS
STRUCTED ANSWERS BOTH IN THEORY & PRACTICALS
NOT THE LEAST – DONOT LOSE YOUR NERVE
63. EDIC 2. CASE DISCUSSION
• 4 CASES
• EACH CASE WILL HAVE 3 OR 4 SCENARIOS
• QUESTIONS TO ASSESS THE BREADTH OF KNOWLEDGE AND NOT THE DEPTH
• PRACTICAL QS ONLY
• NO THEORETICAL QUESTIONS
• DRNB LEVEL PREPARATION IS MORE THAN ENOUGH
• COMMUNICATION SKILL WILL BE ELICITED
64. THINGS WE DO BUT FORGET TO TELL
• WHEN ASKED HOW WILL YOU MANAGE
• DON’T FORGET TO TELL I WILL PUT A LINE , CVC , HD CATH (IF INDICATED )
• DON’T FORGET TO TELL I WILL ADMIT THE PATIENT IN ICU
• WE TEND TO MISS THIS AND JUMP TO FLUIDS , ANTIBIOTICS ETC ETC
• SUCH MINOR THINGS CARRY MARKS
65. OSCE
• LABS – 10 QS
• HYPONATREMIA IS A FAVOURITE
• QUICKLY INTERPRET THE DATA & COME TO A DIAGNOSIS IN THE ALLOWED TIME
• TIME IS THE ISSUE OTHERWISE IT SHOULD BE FINE
67. ECG , GRAPHS , VENTILATOR WAVEFORMS ,
CULTURE REPORTS
• ECG 3 OR 4
• VERY DIFFICULT UNLESS YOU HAVE PRACTISED WELL
• SIMILAR SITUATION WITH VENTILATOR WAVEFORMS
• PRACTICE IT SO THAT YOU CAN DIAGNOSE IT WITHIN THE ALLOTED TIME
68. GOOD MATERIALS FOR EDIC 2
SOLVE ECGS
,VENTILATOR
WAVEFORMS
AS MUCH AS YOU
CAN
THAT’S THE ONLY
WAY TO MASTER IT