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
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
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
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
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
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
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
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
(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.”
Question: would would rash on chest wall indicate?
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
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
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?
Wellen’s sign – 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.