This document provides guidance on evaluating and managing chest pain. It lists common cardiac, pulmonary, aortic, chest wall, and esophageal causes of chest pain. It describes typical versus atypical chest pain characteristics and provides the Modified Wells Criteria for evaluating pulmonary embolism risk. Evaluation involves history, physical exam, EKG, and lab tests. The document reviews two case studies of patients presenting with chest pain and outlines diagnostic and treatment approaches.
A presentatation on Acute coronary syndrome made while in Emergency Department. If you are making a presentation on ACS, you may want to add more on TIMI score as it is important. Some problems with display of pictures/diagrams due to ?conversion problems. Based on AHA Guidelines 2010 and from Harrison's 18th Ed.. Made using OpenOffice.
Severe hypertension that is a potentially life-threatening condition refers to a hypertensive crisis.
Severe hypertension is further classified into hypertensive emergencies or hypertensive urgencies.
Hypertensive emergency refers to a severe hypertension that is associated with new or progressive end-organ damage. In these clinical situations, blood pressure should be reduced immediately to prevent or minimize organ dysfunction.
Hypertensive urgency refers to severe hypertension without evidence of new or worsening end-organ injury.
A hypertensive emergency is hypertension with acute impairment of one or more
organ systems that can result in irreversible organ damage. Especially:-
Central nervous system
Cardiovascular system
Renal system.
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120mmHg and/or systolic blood pressure greater than or equal to 180mmHg.Â
Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.
A brief presentation regarding etiology , clinical features , and management of chronic limb ischemia. It was presented by our unit at Department of surgery , Patna medical college
A presentatation on Acute coronary syndrome made while in Emergency Department. If you are making a presentation on ACS, you may want to add more on TIMI score as it is important. Some problems with display of pictures/diagrams due to ?conversion problems. Based on AHA Guidelines 2010 and from Harrison's 18th Ed.. Made using OpenOffice.
Severe hypertension that is a potentially life-threatening condition refers to a hypertensive crisis.
Severe hypertension is further classified into hypertensive emergencies or hypertensive urgencies.
Hypertensive emergency refers to a severe hypertension that is associated with new or progressive end-organ damage. In these clinical situations, blood pressure should be reduced immediately to prevent or minimize organ dysfunction.
Hypertensive urgency refers to severe hypertension without evidence of new or worsening end-organ injury.
A hypertensive emergency is hypertension with acute impairment of one or more
organ systems that can result in irreversible organ damage. Especially:-
Central nervous system
Cardiovascular system
Renal system.
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120mmHg and/or systolic blood pressure greater than or equal to 180mmHg.Â
Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.
A brief presentation regarding etiology , clinical features , and management of chronic limb ischemia. It was presented by our unit at Department of surgery , Patna medical college
Chest pain Case Presentation with managementMuqtasidkhan
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CASE presentation of chest pain types, causes, investigations, management. cardiac vs non cardiac pain. life threatening chest pain. MI, ACS, PNEUMOTHORAX, PE, GERD, AORTIC DISSECTION.
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
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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.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
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The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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.
Bowmanâs 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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Tom Selleck Health: A Comprehensive Look at the Iconic Actorâs Wellness Journeygreendigital
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Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on:Â Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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.
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
RecomendaçÃĩes da OMS sobre cuidados maternos e neonatais para uma experiÃĒncia pÃŗs-natal positiva.
Em consonÃĸncia com os ODS â Objetivos do Desenvolvimento SustentÃĄvel e a EstratÊgia Global para a SaÃēde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pÃŗs-natais devem expandir-se para alÊm da cobertura e da simples sobrevivÃĒncia, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pÃŗs-natais essenciais e de rotina prestados à s mulheres e aos recÊm-nascidos, com o objetivo final de melhorar a saÃēde e o bem-estar materno e neonatal.
Uma âexperiÃĒncia pÃŗs-natal positivaâ Ê um resultado importante para todas as mulheres que dÃŖo à luz e para os seus recÊm-nascidos, estabelecendo as bases para a melhoria da saÃēde e do bem-estar a curto e longo prazo. Uma experiÃĒncia pÃŗs-natal positiva Ê definida como aquela em que as mulheres, pessoas que gestam, os recÊm-nascidos, os casais, os pais, os cuidadores e as famÃlias recebem informaçÃŖo consistente, garantia e apoio de profissionais de saÃēde motivados; e onde um sistema de saÃēde flexÃvel e com recursos reconheça as necessidades das mulheres e dos bebÃĒs e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendaçÃĩes novas e jÃĄ bem fundamentadas sobre cuidados pÃŗs-natais de rotina para mulheres e neonatos que recebem cuidados no pÃŗs-parto em unidades de saÃēde ou na comunidade, independentemente dos recursos disponÃveis.
à fornecido um conjunto abrangente de recomendaçÃĩes para cuidados durante o perÃodo puerperal, com ÃĒnfase nos cuidados essenciais que todas as mulheres e recÊm-nascidos devem receber, e com a devida atençÃŖo à qualidade dos cuidados; isto Ê, a entrega e a experiÃĒncia do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendaçÃĩes da OMS de 2014 sobre cuidados pÃŗs-natais da mÃŖe e do recÊm-nascido e complementam as atuais diretrizes da OMS sobre a gestÃŖo de complicaçÃĩes pÃŗs-natais.
O estabelecimento da amamentaçÃŖo e o manejo das principais intercorrÃĒncias Ê contemplada.
Recomendamos muito.
Vamos discutir essas recomendaçÃĩes no nosso curso de pÃŗs-graduaçÃŖo em Aleitamento no Instituto Ciclos.
Esta publicaçÃŖo sÃŗ estÃĄ disponÃvel em inglÃĒs atÊ o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
6. Typical vs. Atypical Chest Pain
Typical
ī§ Characterized as
discomfort/pressure rather than
pain
ī§ Time duration >2 mins
ī§ Provoked by activity/exercise
ī§ Radiation (i.e. arms, jaw)
ī§ Does not change with
respiration/position
ī§ Associated with
diaphoresis/nausea
ī§ Relieved by rest/nitroglycerin
ī§ Post Coital
Atypical
ī§ Pain that can be localized with
one finger
ī§ Constant pain lasting for days
ī§ Fleeting pains lasting for a few
seconds
ī§ Pain reproduced by
movement/palpation
8. Evaluation of Chest Pain
Case 1:
ī§ Ask nurse for most current set of vital signs
ī§ Ask nurse to get an EKG
ī§ See the patient!
9. Evaluation of Chest Pain
ī§ Once at bedside, determine if patient is stable or unstable
ī§ Perform focused history and physical exam
ī§ Read and interpret the EKG. Compare EKG to old EKG if
available
ī§ If patient looks unstable or has concerning EKG findings, call
ER/Cardio On call for help
ī§ Write a clinical event note!
10. Evaluation of Chest Pain
ī§focused physical exam for chest pain
ī§ Vital Signs: tachycardia, hypertension/hypotension or hypoxia
ī§ General: Sick appearing, actively having chest pain
ī§ HEENT: JVD, carotid bruits
ī§ Chest: Rales, wheezes or decreased breath sounds
ī§ CVS: New murmurs, reproducible chest pain, s3 gallop
ī§ Abd: Abdominal tenderness, pulsatile mass
ī§ Ext: Edema, peripheral pulses
ī§ Skin: Rash on chest wall
11. Case 1
ī§ 25 years old lady suddenly developed chest pain that is L-sided,
8/10 and worse with breathing. Vital signs: Afebrile, HR 120, BP
110/70, RR 28, O2 sat 89% on 2L (was 95% on RA this morning)
ī§ Physical exam
ī§ Gen â in distress, using accessory muscles of respiration
ī§ Lungs â CTAB, no rales/wheezes
ī§ Heart â tachycardic, nl s1, loud s2, no mumurs
ī§ Abd â soft, NT/ND, active BS
ī§ Ext â b/l LEs warm and well perfused
ī§ Labs:
ī§ CBC wnl, RFP wnl, BNP = 520, D-dimer = positive, Troponin = 0.12
15. Modified Wells Criteria
ī§ Clinical symptoms of DVT (3 points)
ī§ Other diagnoses less likely than PE (1 point)
ī§ Heart Rate >100 (1.5 points)
ī§ Immobilization >/= 3 days or surgery within 4 weeks (1.5 points)
ī§ Previous DVT/PE (1.5 points)
ī§ Hemoptysis (1 point)
ī§ Malignancy (1 point)
ī§ Interpretation:
ī§ >6: high
ī§ 2-6: moderate
ī§ <2: low
16. Next moves
ī§ DDIMER: 95% sensitive, VERY nonspecific
ī§ ABG â Elevated A-a gradient fairly sensitive, highly
nonspecific
ī§ EKG â most commonly nonspecific changes (ST/T wave
changes, etc)
ī§ V/Q scan â helpful in patients with HIGH or LOW pretest
probabilities in whom a CTPE cannot be obtained (eg CKD)
ī§ LE Ultrasound: not sensitive
ī§ CTPE
ī§ Sensitivity 83%
ī§ Specificity 96%
ī§ Moderate - high clinical probability and positive CTPE: 92-96%
chance of PE
17. Pearl
A CT angiogram (important for evaluating for Pulmonary
Embolism or Aortic Dissection) requires EITHER:
1) At least a 20G peripheral IV
OR
2) A Power injectable central line
19. Diagnostic approach is simple if you
suspect PEâĻ
ī§ Probability low: obtain D-DIMER
ī§ If positive: obtain CTPE
ī§ If negative: PE excluded
ī§ Probability moderate or high: obtain CTPE
ī§ If positive: treat
ī§ If negative: PE excluded
20. Acute Pulmonary Embolism
ī§ Stabliize patient
ī§ oxygen
ī§ Fluids if hypotensive!
ī§ Fibrinolytic Therapy if SBP less 90 mmHg
ī§ Anticoagulants
ī§ Preferred: LMWH or Fondaparinux
ī§ Enoxaparin 1.5mg/kg daily or 1mg/kg BID
ī§ Fondaparinux subcutaneous once daily (weight based)
ī§ Alternative: UFH (IV or SC) â select high intensity protocol
ī§ Hemodynamically unstable patients
ī§ High risk of bleeding (reversible)
ī§ GFR < 30
ī§ Can initiate warfarin on same day
ī§ IVC filter an alternative in patients with mod-high bleeding
risk
Management
21. Pearl: If you have a moderate
or high suspicion of PE, you
can start anticoagulation while
awaiting full diagnostic workup
22. PE with hypotension
ī§ Thrombolysis
ī§ Administer over short infusion time
ī§ Catheter based thrombectomy
ī§ For failure of thrombolysis or likelihood of shock/death before
thrombolysis can take effect (hours)
ī§ Surgical thrombectomy
ī§ Failure of above therapies
23. Case 2
ī§Mr. M is a 67 yo man with PMHx of HTN, DLD,
DMT2 and CAD s/p PCI in 2017. He presents
with new onset chest pain x 2 hours that is
retrosternal, 7/10, associated with nausea and
diaphoresis.
24. Case 2
ī§VS: T 37 HR 108 BP 105/60 RR 20 O2 sat 93%
on RA
ī§Physical exam:
ī§Gen â actively having chest pain, diaphoretic
ī§Lungs â crackles at bilateral bases
ī§Heart â tachycardic, nl s1/s2, no mumurs or rub
ī§Rest of the exam benign
ī§Labs: CBC wnl, RFP wnl, Troponin = 0.05
25. Next Steps
ī§ Review EKG
ī§ Review CXR
ī§ Troponin
ī§ SL Nitroglycerin
ī§ ASA Soluble or Chewable
27. Case 2 Diagnosis:
UA/NSTEMI
ī§ EKG changes in Acute Coronary Syndromes:
ī§ ST elevations
ī§ ST depressions
ī§ T wave inversions
ī§ âpseudonormalizationâ â inversion of previously inverted T waves when
compared with old EKG
ī§ New conduction block
ī§ Q waves
ī§ Importance of serial EKG monitoring: sensitivity of single
EKG is only 50% sensitive for acute MI
28.
29. Next steps
ī§ Vitals
ī§ Repeat EKG
ī§ Repeat SL nitro
ī§ Assess patient in person
ī§ Call ER/Cardio On call/Cath Lab Consultant
35. Criteria for type 1 MI
ī§ Detection of a rise and/or fall of cTn values with at least one
value above the 99th percentile URL and with at least one of
the following:
ī§ Symptoms of acute myocardial ischaemia;
ī§ New ischaemic ECG changes;
ī§ Development of pathological Q waves;
ī§ Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality in a pattern consistent with
an ischaemic aetiology;
ī§ Identification of a coronary thrombus by angiography
including intracoronary imaging or by autopsy.a
38. Nitroglycerin contraindicated in
inferior MI with RV infarction
ī§ Other contraindications to NG:
ī§ Preload dependent states
ī§ Inferior MI
ī§ Aortic outflow obstruction (HOCM, severe AS)
ī§ Likelihood of hemodynamic instability
ī§ HR <50 or >100
ī§ SBP<90mmHg or more than 30mmHg below baseline
ī§ Use of PGE inhibitors, NO TELLING
39. Case 3
ī§ You are called on to admit a 65 yo man for ACS rule out.
ī§ Mr Q is a gentleman with a history of DMT2, NASH, remote
NSTEMI, and HTN presenting with severe retrosternal chest
pain. Pain is different than prior MI but is very severe.
Radiates to neck. Began 3 hours ago; has subsided slightly
but is still 8/10 in severity.
40. You take report, quickly review
chart, and go to assess the patient
in the ER.
ī§ VS: T37.1, HR110, BP145/80 in R arm, RR16, Pox 98%RA
ī§ Focused Exam:
ī§ GEN: in discomfort but mentating well
ī§ HEENT mmm, JVP at clavicle
ī§ CV normal s1/s2, no murmurs
ī§ PULM ctab, no w/c/r
ī§ EXTR: cool
ī§ Bilateral BP: 145/80R, 110/60L
ī§ EKG identical to previous EKG which you printed from portal
41.
42.
43. Thoracic aortic dissection
ī§ CT angiography â first line
ī§ 83-100% sensitive, specificity 87-100%
ī§ TEE â second line; good for proximal, cannot visualize
descending aorta well
ī§ MRI â useful for surveillance
Diagnosis
Images:
reference.medscape.com
rwjms1.umdnj.eduen.wikipedia.org
en.wikipedia.org
44. Thoracic aortic dissection
ī§ Hypertension
ī§ Atherosclerosis
ī§ Preexisting aneurysm (known history in 13% of patients)
ī§ Inflammatory conditions affecting aorta (Takayasu, Giant Cell
Arteritis, RA, syphilis)
ī§ Collagen disorders (Marfan, Ehlers-Danlos)
ī§ Bicuspid aortic valve
ī§ Aortic coarctation
ī§ Turner syndrome
ī§ History of CABG, AVR, Cardiac Cath
ī§ High intensity weight lifting
ī§ Cocaine use
ī§ Trauma
Risk Factors
45.
46. Type A Type B
Thoracic aortic dissection
ī§ Surgery!
ī§ Do not delay surgery, even
for LHC
ī§ Beta blockers, titrate to HR
50-60 (labetalol, esmolol)
ī§ BP control (nitroprusside)
ī§ Beta blockers, titrate to HR
50-60 (labetalol, esmolol)
ī§ BP control â add
nitroprusside or similar agent
to SBP goal 100-120mmHg
ī§ Surgery for those with end
organ damage or those who
do not respond to medical
therapy
ī§ Watch for hypotension â give
fluids if needed, consider
tamponade, MI, or rupture as
complications if hypotensive
Management
47.
48. Case 4
ī§53 yo M with chest pain and EKG abnormalities
ī§PMHx:
ī§ HTN
ī§ Dyslipidemia
ī§You go see the patient and he tells you that
he has had this chest pain for ~2 days, but
it has progressively gotten worse. His
chest pain is worse with breathing. He
notes a recent viral URI.
49. Case 4
ī§ VS: T 37.9 HR 104 BP 140/76 RR 20 O2 sat 95% on RA
ī§ Physical exam:
ī§ Gen â in mild distress due to chest pain, leaning forward while in
bed
ī§ Lungs â CTAB
ī§ Chest wall â no visible rash, chest wall NT to palpation
ī§ Heart â tachycardic, nl s1/s2, no rub
ī§ Rest of physical exam benign
ī§ Labs:
ī§ WBC = 14, RFP wnl, AMI panel x 1 = negative
ī§ CXR = negative
51. Case 4 - Pericarditis
ī§Refers to inflammation of pericardial sac
ī§Idiopathic pericarditis typically preceded by
viral prodrome, i.e. flu-like symptoms
ī§Typically, patients have sharp, pleuritic
chest pain relieved by sitting up or leaning
forward
54. Case 4 - Pericarditis
ī§ Diagnostic criteria
UpToDate 2012
55. Case 4 â Pericarditis
ī§ High risk features:
ī§ Fever (>38ÂēC [100.4ÂēF]) and leukocytosis
ī§ Evidence suggesting cardiac tamponade
ī§ A large pericardial effusion (ie, an echo-free space of more than
20 mm)
ī§ Immunosuppressed state
ī§ A history of therapy with vitamin K antagonists (eg warfarin)
ī§ Acute trauma
ī§ Failure to respond within seven days to NSAID therapy
ī§ Elevated cardiac troponin, which suggests myopericarditis
56. Case 4 - Pericarditis
ī§ Treatment
UpToDate 2012
57. Case 5
ī§ This is a 45 yro M with PMHx of rheumatoid arthritis who
presented with progressive sob. He was found to have a R-
sided pleural effusion and underwent an US guided
thoracentesis with removal of 1.5 liters of pleural fluid. Two
hours after his procedure, he develops new onset R-sided
chest pain
59. Case 5 - Pneumothorax
ī§ Management of Pneumothorax
ī§ 100% O2 and observation in stable patients for PTX < 3 cm in
size
ī§ Needle aspiration in stable patients for PTX >3 cm
ī§ Chest tube placement if PTX >3 cm and if needle aspiration fails
ī§ Chest tube placement in unstable patients
In keeping with this being intern bootcamp, Iâm going to focus on common scenarios youâll encounter in hospitalized patients
Iâll try to keep this relevant, with some lessions Iâve learned along the way
MI
PE
Dissection (20G IV!)
Costocondiritis/musculoskeletal
Esophageal Spasm
Acute Chest
PNA
pericarditis
Pleuritis
Heartburn
RUQ pathology
Panic attack
Cocaine chest pain
Aortic Stenosis
Myocarditis
Eosinophilic Esophagitis
Esophageal Rupture/Perforation
Asthma/COPD
Pneumothorax
Pearls:
donât accept âchest painâ â could be abdominal, patients havenât read the anatomy books! (story of kidney stones)
Need 20G IV or power injectable central line for contrast â important for PE and TAA
MI: continued chest pain on floor in NSTEMI
TPA in PE
(just because the ER says it is chest pain doesnât mean itâs not abdominal pain)
If the patient can localize pain with 1 finger, less likely to be ACS
Many patients will indicate abdomen but say âchest.â
Question: would would rash on chest wall indicate?
ABG â A-a gradient can be normal in ~6% of patients with PE,
EKG â 70% had changes, in one study
LE ultrasound: only 29% of patients with known PE had + u/s in one study. False positive ~3%.
Can help to define clot burden in cases of known PE
Echo: only 30-40% sensitive
Echocardiolography â useful for suspected massive/submassive PE where use of thrombolytics is in question.
V/Q Scan:
Useful in the following scenarios:
Renal insufficiency
Contrast allergy
Morbid obesity
Inconclusive CTPE
- Helpful scenarios:
High clinical probability with high likelihood V/Q: 95% chance of PE
Low clinical probability with low probability V/Q: 4% chance of PE
Normal V/Q essentially excludes PE
Other situations, V/Q scan is insufficient to diagnose or exclude PE
Fluids important particularly with submassive/massive PE causing RH failure â patients are preload dependent
Choice of anticoagulant: ACCP recommends LMWH or Fonda over UFH, evidence level 2B for LMWH, 2C for fonda
Once daily dosing for LMWH typically OK â use BID for patients with cancer, extensive clot burden, or higher BMI (>30)
Fondaparinux dosingâ 5mg for patients <50kg, 7.5mg for patients between 50-100kg, and 10mg daily for patients >100mg
IV heparin protocol is useful for:
Hemodynamically unstable patients (excluded from trials of LMWH)
High risk of bleeding, because IV heparin can be shut off, and reversed with protamine sulfate
GFR < 30 -> UFH can be more easily monitored and adjusted
Patients in whom thrombolytics are being considered â can shut off IV heparin while thrombolytics being infused, to avoid simultaneous administration of thrombolytics and anticoagulants
Morbidly obese patients â subcu absorption of LMWH and Fonda may be affected
Bleeding risk
-one risk factor: 3.2% in first 3 months, 1.6 per year thereafter
-Two or more risk factors: 12.8% in first 3 months, 6.5 per year thereafter
-contrast with risk of recurrent PE 25% in those who fail to achieve ther
Bleeding risk factors:
Age >65
Thrombocytopenia
Recent surgery
Poor med adherence
DM
Previous stroke
Anemia
Cancer
Renal failure
Liver failure
Alcohol abuse
Per ACCP algorithm:
High clinical suspicion of PE: start anticoagulation, then proceed to diagnostic evaluation
Moderate clinical suspicion of PE: start anticoagulation if diagnostic eval anticipated to take more than 4 hours
Low clinical suspicion of PE: start anticoagulation if diagnostic eval anticipated to take more than 24 hours
Can you make a diagnosis at this point?
What is your diagnosis?
Wellenâs sign â Deep TWI in V4-V5 = tight proximal LAD
Symptoms: decrased perfusion based on extent of dissection
Carotids: neuro sx with decreased consciousness, stroke, paraplegia
LE ischemia
Exam
BP: both arms (sens/spec?)
Cool extremities
Pain to back
CXR: wide mediastinum
Widened aortic knob
CXR findings:
-mediastinal widening in 56% (type B) and 63% (type A);
-pleural effusion in 19%
-normal in 11% (type A) and 16% (type B)
TEE: advantage, can diagnose aortic incompetence
Disadvantage; cannot visualize descending aorta
78% sensitive, specificity 83% for Type A dissections in one prospective cohort trial
Another meta-analysis found
->Relate anecdote about patient in ER
Medical Management:
-Begin with IV beta-blockade to goal HR 50-60
-If SBP fails to reach 100-120mmHg with beta blockade alone, and patient not showing signs of hypoperfusion (particularly altered mental status) then add nitroprusside to reach SBP goal
Early Repol: J point elevated, ST segment otherwise normal
Effusion: present in 180/300 in one series (60%); of those, 79% small and 10% moderate. Tamponade in only 5%.
In a series of 300 patients, 85% low risk and none had serious complications
Nitrogen washout: In animal models, administration of 100% FiO2 increased reabsorption of PTX 6-fold. The reason this works is likely due to the altered gradient in pressure of dissolved gas in the distal capillary bed. A patient on room air might have a partial pressure of nitrogen of ~570mmHg which is present in both arterial and post-capillary samples. A patient on 100%FiO2 has a partial pressure of nitrogen of zero, since nitrogen has been replaced by oxygen. The arterial PO2 might be ~650mmHg in such a patient, but because of the efficient uptake of dissolved O2 by body tissue, the distal capillary PO2 might only be a small amount higher than in a patient on room air (55mmHg vs 40mmHg.) This provides a substantial pressure gradient for reabsorption of the air in the pneumothorax.