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Approach to Chest Pain
2020
Dull ache
Ihab suliman
MBBS ECFMG MRCP(UK) MRCP
specialty(Endocrinology &DM) ABcv FESC CBNC
0505244473
4475
Ihab.suliman@gmail.com
Differential
 Cardiac
 MI
 Pericarditis
 Myocarditis
 Aortic Stenosis
 Pulmonary
 PE
 PNA
 Asthma/COPD
 Acute Chest Syndrome
 Pleura
 Pleuritis
 Pneumothorax
 Aorta
 Dissection
 Perforated ulcer
 Chest wall
 Costocondiritis/musculoskeletal
 Esophagus
 Esophageal Spasm
 Eosinophilic Esophagitis
 Esophageal
Rupture/Perforation
 GERD
 Mediastinitis
 RUQ pathology
 Panic attack
Lethal Causes of Chest Pain
1- Acute Coronary Syndrome
2- Acute Aortic dissection Type A.
3-Massive Pulmonary Embolism
4-Pericardial Tamponade
5-Esophageal Rupture
6-Tension Pneumothorax
Pearl: ALWAYS have
the patient point to
the pain!
Typical vs. Atypical Chest Pain
Typical
 Characterized as
discomfort/pressure rather than
pain
 Time duration >2 mins
 Provoked by activity/exercise
 Radiation (i.e. arms, jaw)
 Does not change with
respiration/position
 Associated with
diaphoresis/nausea
 Relieved by rest/nitroglycerin
 Post Coital
Atypical
 Pain that can be localized with
one finger
 Constant pain lasting for days
 Fleeting pains lasting for a few
seconds
 Pain reproduced by
movement/palpation
Typical vs. Atypical Chest Pain
UpToDate 2012
Evaluation of Chest Pain
Case 1:
 Ask nurse for most current set of vital signs
 Ask nurse to get an EKG
 See the patient!
Evaluation of Chest Pain
 Once at bedside, determine if patient is stable or unstable
 Perform focused history and physical exam
 Read and interpret the EKG. Compare EKG to old EKG if
available
 If patient looks unstable or has concerning EKG findings, call
ER/Cardio On call for help
 Write a clinical event note!
Evaluation of Chest Pain
focused physical exam for chest pain
 Vital Signs: tachycardia, hypertension/hypotension or hypoxia
 General: Sick appearing, actively having chest pain
 HEENT: JVD, carotid bruits
 Chest: Rales, wheezes or decreased breath sounds
 CVS: New murmurs, reproducible chest pain, s3 gallop
 Abd: Abdominal tenderness, pulsatile mass
 Ext: Edema, peripheral pulses
 Skin: Rash on chest wall
Case 1
 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)
 Physical exam
 Gen – in distress, using accessory muscles of respiration
 Lungs – CTAB, no rales/wheezes
 Heart – tachycardic, nl s1, loud s2, no mumurs
 Abd – soft, NT/ND, active BS
 Ext – b/l LEs warm and well perfused
 Labs:
 CBC wnl, RFP wnl, BNP = 520, D-dimer = positive, Troponin = 0.12
Case 1
Case 1
Differential
 Cardiac
 MI
 Pericarditis
 Myocarditis
 Pulmonary
 PE
 PNA
 Asthma/COPD
 Acute Chest Syndrome
 Pleura
 Pleuritis
 Pneumothorax
 Aorta
 Dissection
 Perforated ulcer
 Chest wall
 Costocondiritis/musculoskeletal
 Esophagus
 Esophageal Spasm
 Eosinophilic Esophagitis
 Esophageal
Rupture/Perforation
 GERD
 Mediastinitis
 RUQ pathology
 Panic attack
Modified Wells Criteria
 Clinical symptoms of DVT (3 points)
 Other diagnoses less likely than PE (1 point)
 Heart Rate >100 (1.5 points)
 Immobilization >/= 3 days or surgery within 4 weeks (1.5 points)
 Previous DVT/PE (1.5 points)
 Hemoptysis (1 point)
 Malignancy (1 point)
 Interpretation:
 >6: high
 2-6: moderate
 <2: low
Next moves
 DDIMER: 95% sensitive, VERY nonspecific
 ABG – Elevated A-a gradient fairly sensitive, highly
nonspecific
 EKG – most commonly nonspecific changes (ST/T wave
changes, etc)
 V/Q scan – helpful in patients with HIGH or LOW pretest
probabilities in whom a CTPE cannot be obtained (eg CKD)
 LE Ultrasound: not sensitive
 CTPE
 Sensitivity 83%
 Specificity 96%
 Moderate - high clinical probability and positive CTPE: 92-96%
chance of PE
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
Case 1
Diagnostic approach is simple if you
suspect PE…
 Probability low: obtain D-DIMER
 If positive: obtain CTPE
 If negative: PE excluded
 Probability moderate or high: obtain CTPE
 If positive: treat
 If negative: PE excluded
Acute Pulmonary Embolism
 Stabliize patient
 oxygen
 Fluids if hypotensive!
 Fibrinolytic Therapy if SBP less 90 mmHg
 Anticoagulants
 Preferred: LMWH or Fondaparinux
 Enoxaparin 1.5mg/kg daily or 1mg/kg BID
 Fondaparinux subcutaneous once daily (weight based)
 Alternative: UFH (IV or SC) – select high intensity protocol
 Hemodynamically unstable patients
 High risk of bleeding (reversible)
 GFR < 30
 Can initiate warfarin on same day
 IVC filter an alternative in patients with mod-high bleeding
risk
Management
Pearl: If you have a moderate
or high suspicion of PE, you
can start anticoagulation while
awaiting full diagnostic workup
PE with hypotension
 Thrombolysis
 Administer over short infusion time
 Catheter based thrombectomy
 For failure of thrombolysis or likelihood of shock/death before
thrombolysis can take effect (hours)
 Surgical thrombectomy
 Failure of above therapies
Case 2
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.
Case 2
VS: T 37 HR 108 BP 105/60 RR 20 O2 sat 93%
on RA
Physical exam:
Gen – actively having chest pain, diaphoretic
Lungs – crackles at bilateral bases
Heart – tachycardic, nl s1/s2, no mumurs or rub
Rest of the exam benign
Labs: CBC wnl, RFP wnl, Troponin = 0.05
Next Steps
 Review EKG
 Review CXR
 Troponin
 SL Nitroglycerin
 ASA Soluble or Chewable
Case 2
Case 2 Diagnosis:
UA/NSTEMI
 EKG changes in Acute Coronary Syndromes:
 ST elevations
 ST depressions
 T wave inversions
 “pseudonormalization” – inversion of previously inverted T waves when
compared with old EKG
 New conduction block
 Q waves
 Importance of serial EKG monitoring: sensitivity of single
EKG is only 50% sensitive for acute MI
Next steps
 Vitals
 Repeat EKG
 Repeat SL nitro
 Assess patient in person
 Call ER/Cardio On call/Cath Lab Consultant
Trivia
Criteria for type 1 MI
 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:
 Symptoms of acute myocardial ischaemia;
 New ischaemic ECG changes;
 Development of pathological Q waves;
 Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality in a pattern consistent with
an ischaemic aetiology;
 Identification of a coronary thrombus by angiography
including intracoronary imaging or by autopsy.a
What typical ACS med should you
NOT give this patient?
Nitroglycerin contraindicated in
inferior MI with RV infarction
 Other contraindications to NG:
 Preload dependent states
 Inferior MI
 Aortic outflow obstruction (HOCM, severe AS)
 Likelihood of hemodynamic instability
 HR <50 or >100
 SBP<90mmHg or more than 30mmHg below baseline
 Use of PGE inhibitors, NO TELLING
Case 3
 You are called on to admit a 65 yo man for ACS rule out.
 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.
You take report, quickly review
chart, and go to assess the patient
in the ER.
 VS: T37.1, HR110, BP145/80 in R arm, RR16, Pox 98%RA
 Focused Exam:
 GEN: in discomfort but mentating well
 HEENT mmm, JVP at clavicle
 CV normal s1/s2, no murmurs
 PULM ctab, no w/c/r
 EXTR: cool
 Bilateral BP: 145/80R, 110/60L
 EKG identical to previous EKG which you printed from portal
Thoracic aortic dissection
 CT angiography – first line
 83-100% sensitive, specificity 87-100%
 TEE – second line; good for proximal, cannot visualize
descending aorta well
 MRI – useful for surveillance
Diagnosis
Images:
reference.medscape.com
rwjms1.umdnj.eduen.wikipedia.org
en.wikipedia.org
Thoracic aortic dissection
 Hypertension
 Atherosclerosis
 Preexisting aneurysm (known history in 13% of patients)
 Inflammatory conditions affecting aorta (Takayasu, Giant Cell
Arteritis, RA, syphilis)
 Collagen disorders (Marfan, Ehlers-Danlos)
 Bicuspid aortic valve
 Aortic coarctation
 Turner syndrome
 History of CABG, AVR, Cardiac Cath
 High intensity weight lifting
 Cocaine use
 Trauma
Risk Factors
Type A Type B
Thoracic aortic dissection
 Surgery!
 Do not delay surgery, even
for LHC
 Beta blockers, titrate to HR
50-60 (labetalol, esmolol)
 BP control (nitroprusside)
 Beta blockers, titrate to HR
50-60 (labetalol, esmolol)
 BP control – add
nitroprusside or similar agent
to SBP goal 100-120mmHg
 Surgery for those with end
organ damage or those who
do not respond to medical
therapy
 Watch for hypotension – give
fluids if needed, consider
tamponade, MI, or rupture as
complications if hypotensive
Management
Case 4
53 yo M with chest pain and EKG abnormalities
PMHx:
 HTN
 Dyslipidemia
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.
Case 4
 VS: T 37.9 HR 104 BP 140/76 RR 20 O2 sat 95% on RA
 Physical exam:
 Gen – in mild distress due to chest pain, leaning forward while in
bed
 Lungs – CTAB
 Chest wall – no visible rash, chest wall NT to palpation
 Heart – tachycardic, nl s1/s2, no rub
 Rest of physical exam benign
 Labs:
 WBC = 14, RFP wnl, AMI panel x 1 = negative
 CXR = negative
Case 4
 EKG on admission:
Case 4 - Pericarditis
Refers to inflammation of pericardial sac
Idiopathic pericarditis typically preceded by
viral prodrome, i.e. flu-like symptoms
Typically, patients have sharp, pleuritic
chest pain relieved by sitting up or leaning
forward
Goyle 2002
Case 4 - Pericarditis
Goyle 2002
Case 4 - Pericarditis
 Diagnostic criteria
UpToDate 2012
Case 4 – Pericarditis
 High risk features:
 Fever (>38ºC [100.4ºF]) and leukocytosis
 Evidence suggesting cardiac tamponade
 A large pericardial effusion (ie, an echo-free space of more than
20 mm)
 Immunosuppressed state
 A history of therapy with vitamin K antagonists (eg warfarin)
 Acute trauma
 Failure to respond within seven days to NSAID therapy
 Elevated cardiac troponin, which suggests myopericarditis
Case 4 - Pericarditis
 Treatment
UpToDate 2012
Case 5
 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
Case 5
Case 5 - Pneumothorax
 Management of Pneumothorax
 100% O2 and observation in stable patients for PTX < 3 cm in
size
 Needle aspiration in stable patients for PTX >3 cm
 Chest tube placement if PTX >3 cm and if needle aspiration fails
 Chest tube placement in unstable patients
Thank You very much

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Approach to chest pain 3 17- 2020

  • 1. Approach to Chest Pain 2020 Dull ache Ihab suliman MBBS ECFMG MRCP(UK) MRCP specialty(Endocrinology &DM) ABcv FESC CBNC 0505244473 4475 Ihab.suliman@gmail.com
  • 2. Differential  Cardiac  MI  Pericarditis  Myocarditis  Aortic Stenosis  Pulmonary  PE  PNA  Asthma/COPD  Acute Chest Syndrome  Pleura  Pleuritis  Pneumothorax  Aorta  Dissection  Perforated ulcer  Chest wall  Costocondiritis/musculoskeletal  Esophagus  Esophageal Spasm  Eosinophilic Esophagitis  Esophageal Rupture/Perforation  GERD  Mediastinitis  RUQ pathology  Panic attack
  • 3.
  • 4. Lethal Causes of Chest Pain 1- Acute Coronary Syndrome 2- Acute Aortic dissection Type A. 3-Massive Pulmonary Embolism 4-Pericardial Tamponade 5-Esophageal Rupture 6-Tension Pneumothorax
  • 5. Pearl: ALWAYS have the patient point to the pain!
  • 6. Typical vs. Atypical Chest Pain Typical  Characterized as discomfort/pressure rather than pain  Time duration >2 mins  Provoked by activity/exercise  Radiation (i.e. arms, jaw)  Does not change with respiration/position  Associated with diaphoresis/nausea  Relieved by rest/nitroglycerin  Post Coital Atypical  Pain that can be localized with one finger  Constant pain lasting for days  Fleeting pains lasting for a few seconds  Pain reproduced by movement/palpation
  • 7. Typical vs. Atypical Chest Pain UpToDate 2012
  • 8. Evaluation of Chest Pain Case 1:  Ask nurse for most current set of vital signs  Ask nurse to get an EKG  See the patient!
  • 9. Evaluation of Chest Pain  Once at bedside, determine if patient is stable or unstable  Perform focused history and physical exam  Read and interpret the EKG. Compare EKG to old EKG if available  If patient looks unstable or has concerning EKG findings, call ER/Cardio On call for help  Write a clinical event note!
  • 10. Evaluation of Chest Pain focused physical exam for chest pain  Vital Signs: tachycardia, hypertension/hypotension or hypoxia  General: Sick appearing, actively having chest pain  HEENT: JVD, carotid bruits  Chest: Rales, wheezes or decreased breath sounds  CVS: New murmurs, reproducible chest pain, s3 gallop  Abd: Abdominal tenderness, pulsatile mass  Ext: Edema, peripheral pulses  Skin: Rash on chest wall
  • 11. Case 1  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)  Physical exam  Gen – in distress, using accessory muscles of respiration  Lungs – CTAB, no rales/wheezes  Heart – tachycardic, nl s1, loud s2, no mumurs  Abd – soft, NT/ND, active BS  Ext – b/l LEs warm and well perfused  Labs:  CBC wnl, RFP wnl, BNP = 520, D-dimer = positive, Troponin = 0.12
  • 14. Differential  Cardiac  MI  Pericarditis  Myocarditis  Pulmonary  PE  PNA  Asthma/COPD  Acute Chest Syndrome  Pleura  Pleuritis  Pneumothorax  Aorta  Dissection  Perforated ulcer  Chest wall  Costocondiritis/musculoskeletal  Esophagus  Esophageal Spasm  Eosinophilic Esophagitis  Esophageal Rupture/Perforation  GERD  Mediastinitis  RUQ pathology  Panic attack
  • 15. Modified Wells Criteria  Clinical symptoms of DVT (3 points)  Other diagnoses less likely than PE (1 point)  Heart Rate >100 (1.5 points)  Immobilization >/= 3 days or surgery within 4 weeks (1.5 points)  Previous DVT/PE (1.5 points)  Hemoptysis (1 point)  Malignancy (1 point)  Interpretation:  >6: high  2-6: moderate  <2: low
  • 16. Next moves  DDIMER: 95% sensitive, VERY nonspecific  ABG – Elevated A-a gradient fairly sensitive, highly nonspecific  EKG – most commonly nonspecific changes (ST/T wave changes, etc)  V/Q scan – helpful in patients with HIGH or LOW pretest probabilities in whom a CTPE cannot be obtained (eg CKD)  LE Ultrasound: not sensitive  CTPE  Sensitivity 83%  Specificity 96%  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 PE…  Probability low: obtain D-DIMER  If positive: obtain CTPE  If negative: PE excluded  Probability moderate or high: obtain CTPE  If positive: treat  If negative: PE excluded
  • 20. Acute Pulmonary Embolism  Stabliize patient  oxygen  Fluids if hypotensive!  Fibrinolytic Therapy if SBP less 90 mmHg  Anticoagulants  Preferred: LMWH or Fondaparinux  Enoxaparin 1.5mg/kg daily or 1mg/kg BID  Fondaparinux subcutaneous once daily (weight based)  Alternative: UFH (IV or SC) – select high intensity protocol  Hemodynamically unstable patients  High risk of bleeding (reversible)  GFR < 30  Can initiate warfarin on same day  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  Thrombolysis  Administer over short infusion time  Catheter based thrombectomy  For failure of thrombolysis or likelihood of shock/death before thrombolysis can take effect (hours)  Surgical thrombectomy  Failure of above therapies
  • 23. Case 2 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 VS: T 37 HR 108 BP 105/60 RR 20 O2 sat 93% on RA Physical exam: Gen – actively having chest pain, diaphoretic Lungs – crackles at bilateral bases Heart – tachycardic, nl s1/s2, no mumurs or rub Rest of the exam benign Labs: CBC wnl, RFP wnl, Troponin = 0.05
  • 25. Next Steps  Review EKG  Review CXR  Troponin  SL Nitroglycerin  ASA Soluble or Chewable
  • 27. Case 2 Diagnosis: UA/NSTEMI  EKG changes in Acute Coronary Syndromes:  ST elevations  ST depressions  T wave inversions  “pseudonormalization” – inversion of previously inverted T waves when compared with old EKG  New conduction block  Q waves  Importance of serial EKG monitoring: sensitivity of single EKG is only 50% sensitive for acute MI
  • 28.
  • 29. Next steps  Vitals  Repeat EKG  Repeat SL nitro  Assess patient in person  Call ER/Cardio On call/Cath Lab Consultant
  • 31.
  • 32.
  • 33.
  • 34.
  • 35. Criteria for type 1 MI  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:  Symptoms of acute myocardial ischaemia;  New ischaemic ECG changes;  Development of pathological Q waves;  Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology;  Identification of a coronary thrombus by angiography including intracoronary imaging or by autopsy.a
  • 36.
  • 37. What typical ACS med should you NOT give this patient?
  • 38. Nitroglycerin contraindicated in inferior MI with RV infarction  Other contraindications to NG:  Preload dependent states  Inferior MI  Aortic outflow obstruction (HOCM, severe AS)  Likelihood of hemodynamic instability  HR <50 or >100  SBP<90mmHg or more than 30mmHg below baseline  Use of PGE inhibitors, NO TELLING
  • 39. Case 3  You are called on to admit a 65 yo man for ACS rule out.  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.  VS: T37.1, HR110, BP145/80 in R arm, RR16, Pox 98%RA  Focused Exam:  GEN: in discomfort but mentating well  HEENT mmm, JVP at clavicle  CV normal s1/s2, no murmurs  PULM ctab, no w/c/r  EXTR: cool  Bilateral BP: 145/80R, 110/60L  EKG identical to previous EKG which you printed from portal
  • 41.
  • 42.
  • 43. Thoracic aortic dissection  CT angiography – first line  83-100% sensitive, specificity 87-100%  TEE – second line; good for proximal, cannot visualize descending aorta well  MRI – useful for surveillance Diagnosis Images: reference.medscape.com rwjms1.umdnj.eduen.wikipedia.org en.wikipedia.org
  • 44. Thoracic aortic dissection  Hypertension  Atherosclerosis  Preexisting aneurysm (known history in 13% of patients)  Inflammatory conditions affecting aorta (Takayasu, Giant Cell Arteritis, RA, syphilis)  Collagen disorders (Marfan, Ehlers-Danlos)  Bicuspid aortic valve  Aortic coarctation  Turner syndrome  History of CABG, AVR, Cardiac Cath  High intensity weight lifting  Cocaine use  Trauma Risk Factors
  • 45.
  • 46. Type A Type B Thoracic aortic dissection  Surgery!  Do not delay surgery, even for LHC  Beta blockers, titrate to HR 50-60 (labetalol, esmolol)  BP control (nitroprusside)  Beta blockers, titrate to HR 50-60 (labetalol, esmolol)  BP control – add nitroprusside or similar agent to SBP goal 100-120mmHg  Surgery for those with end organ damage or those who do not respond to medical therapy  Watch for hypotension – give fluids if needed, consider tamponade, MI, or rupture as complications if hypotensive Management
  • 47.
  • 48. Case 4 53 yo M with chest pain and EKG abnormalities PMHx:  HTN  Dyslipidemia 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  VS: T 37.9 HR 104 BP 140/76 RR 20 O2 sat 95% on RA  Physical exam:  Gen – in mild distress due to chest pain, leaning forward while in bed  Lungs – CTAB  Chest wall – no visible rash, chest wall NT to palpation  Heart – tachycardic, nl s1/s2, no rub  Rest of physical exam benign  Labs:  WBC = 14, RFP wnl, AMI panel x 1 = negative  CXR = negative
  • 50. Case 4  EKG on admission:
  • 51. Case 4 - Pericarditis Refers to inflammation of pericardial sac Idiopathic pericarditis typically preceded by viral prodrome, i.e. flu-like symptoms Typically, patients have sharp, pleuritic chest pain relieved by sitting up or leaning forward
  • 53. Case 4 - Pericarditis Goyle 2002
  • 54. Case 4 - Pericarditis  Diagnostic criteria UpToDate 2012
  • 55. Case 4 – Pericarditis  High risk features:  Fever (>38ºC [100.4ºF]) and leukocytosis  Evidence suggesting cardiac tamponade  A large pericardial effusion (ie, an echo-free space of more than 20 mm)  Immunosuppressed state  A history of therapy with vitamin K antagonists (eg warfarin)  Acute trauma  Failure to respond within seven days to NSAID therapy  Elevated cardiac troponin, which suggests myopericarditis
  • 56. Case 4 - Pericarditis  Treatment UpToDate 2012
  • 57. Case 5  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  Management of Pneumothorax  100% O2 and observation in stable patients for PTX < 3 cm in size  Needle aspiration in stable patients for PTX >3 cm  Chest tube placement if PTX >3 cm and if needle aspiration fails  Chest tube placement in unstable patients

Editor's Notes

  1. In keeping with this being intern bootcamp, I’m going to focus on common scenarios you’ll encounter in hospitalized patients I’ll try to keep this relevant, with some lessions I’ve 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: don’t accept “chest pain” – could be abdominal, patients haven’t read the anatomy books! (story of kidney stones) Need 20G IV or power injectable central line for contrast – important for PE and TAA MI: continued chest pain on floor in NSTEMI TPA in PE
  2. (just because the ER says it is chest pain doesn’t mean it’s not abdominal pain) If the patient can localize pain with 1 finger, less likely to be ACS Many patients will indicate abdomen but say “chest.”
  3. Question: would would rash on chest wall indicate?
  4. ABG – A-a gradient can be normal in ~6% of patients with PE, EKG – 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 – 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
  5. Fluids important particularly with submassive/massive PE causing RH failure – 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 – use BID for patients with cancer, extensive clot burden, or higher BMI (>30) Fondaparinux dosing– 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 – can shut off IV heparin while thrombolytics being infused, to avoid simultaneous administration of thrombolytics and anticoagulants Morbidly obese patients – 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
  6. 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
  7. Can you make a diagnosis at this point? What is your diagnosis?
  8. Wellen’s sign – Deep TWI in V4-V5 = tight proximal LAD
  9. Nitroglycerin! Inferior MI = RV infarct -> RV failure -> preload dependence
  10. 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
  11. 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)
  12. 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
  13. 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
  14. Early Repol: J point elevated, ST segment otherwise normal
  15. Effusion: present in 180/300 in one series (60%); of those, 79% small and 10% moderate. Tamponade in only 5%.
  16. In a series of 300 patients, 85% low risk and none had serious complications
  17. 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.