Transcript Chest Pain

Chest Pain
William Beaumont Hospital
Department of Emergency Medicine
Shanna Jones, MD
The Things That Kill…
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Acute MI
Pulmonary Embolus (PE)
Pneumothorax (PTX)
Aortic Dissection
Esophageal Rupture (Boerhaave’s)
Let’s dive right in…
Chest Pain: What is it?
65 y/o male complains of substernal chest
pressure and tightening that radiates to his
left arm, shortness of breath, diaphoresis,
and nausea that started while working in
the yard.
PMHx: HTN, high cholesterol
Soc: + tobacco
FHx: father died at 62 of MI
Chest Pain: What is it?
86 y/o female presents with generalized
weakness, mental status changes,
vomiting, epigastric pain, and syncope
after her last episode of vomiting.
There is no other history as the NH did not
feel it was necessary to send her records.
Chest Pain: What is it?
36 y/o obese, diabetic male presents with
weakness, fatigue. shortness of breath
whenever he gets off the couch, and “just
not feeling right, doc.”
PMHx: diabetes since his teens, HTN, high
cholesterol
FHx: Mom – HTN; Dad – “had a bad heart”
Acute Coronary Syndrome (ACS)
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Includes USA, NSTEMI, STEMI
Leading cause of death among adults in
the US (about 1 million, 2006)
6 million people present to the ER per
year with chest pain
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2 million of these receive the diagnosis of ACS
Cost of doing business: $100-120 billion
Risk Factors for CAD – Typical
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Male
Older Age
Tobacco
HTN
DM
High Cholesterol
FHx
Cocaine
Artificial/early menopause
Risk Factors for CAD – Atypical
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DM
Elderly
Female
Nonwhite
Dementia
No history of MI
No history of high cholesterol
CHF
CVA
Unstable Angina (USA) Defined
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New onset angina occurring with minimal
exertion or at rest, worsening of previous
angina, increased frequency or duration of
attack, and resistance to previous treatment
ECG: normal/unchanged, nonspecific ST
segment changes, or T wave inversions
Acute Myocardial Infarction (AMI)
Definition
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Rise and fall of cardiac biomarkers with the
following
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Ischemic symptoms (critical vessel stenosis with
increased myocardial work load or plaque rupture)
Development of Q waves on ECG
ST segment elevation or depression (STEMI &
NSTEMI)
Coronary artery intervention (lytics or cath lab)
NSTEMI Definition
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Positive cardiac enzymes in the
appropriate clinical scenario without ST
elevation on the ECG
ECG – normal, T wave inversions, ST
segment depressions
ECG Findings of ACS
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Hyperacute T waves
ST segment elevation of 1 mm
ST segment depression – NSTEMI vs
reciprocal changes
T wave inversions – initial presentation or
evolving infarct
Q waves – may emerge in the initial hour,
but usually develop at 8-12 hours
Normal ECG
Injury Patterns on the ECG
Anterior wall MI: ST segment elevation V1-V4
Vessel: LAD
Injury Patterns on the ECG
Injury Patterns on the ECG
Lateral Wall MI: I, aVL, V5, V6
Vessel: variable perfusion of LAD, RCA, LCx
Injury Patterns on the ECG
Anterolateral with reciprocal changes
Vessels: LAD and 1st diagonal branch
Injury Patterns on the ECG
Inferior wall MI: II, III, aVF
Vessel: 90% RCA, 10% LCx
Injury Patterns on the ECG
Posterior Wall MI: V1-V3 depression, tall upright
T, tall wide R wave, R/S ratio greater than 1
Vessel: RCA, PDA, LCx
Injury Patterns on the ECG
Inferior Wall MI with Posterior Wall MI: V1V3 depression, tall upright T, tall wide R wave,
R/S ratio greater than 1
Vessel: RCA, PDA, LCx
Moving on…
What do you want to order in
addition to an ECG for a patient
presenting with chest pain,
suspected ACS?
Initial Evaluation
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IV, O2, monitor
Focused H&P
CBC
Chem 7
CK-MB, troponin, myoglobin
CXR
PT/PTT
Possible D-dimer
? Repeat ECG
Treatment in the ED: STEMI
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Activate the acute MI page and cath lab
ASA 325mg PO – proven to save lives
NTG SL and gtt – reduces preload>afterload,
dilates coronary arteries
Heparin 60 U/kg bolus then 16 U/kg/hour
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? Beta Blocker
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Treatment in the ED: STEMI
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Morphine – for persistent pain or anxiety to
reduce O2 need, weak sympathetic blocker,
preload reducer through venous dilation
Glycoprotein IIb/IIIA inhibitors – started in
the EC or cath lab for those patients
undergoing mechanical coronary intervention
Plavix – in consultation with the cardiologist
as it prohibits CABG for 5 days
Treatment in the ED: STEMI
Reperfusion Therapy
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PCI – 90 minute rule
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Most people are eligible
Decreased risk of bleeding and stroke
Higher initial reperfusion rates
Defines coronary vasculature and allows for
treatment vs. surgical referral
t-PA – when PCI cannot be achieved in 90
minutes or is not available
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0-12 hours after symptom onset
NTG
When to think twice?
NTG: Be cautious…
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Bradycardia
Hypotension
Inferior or posterior wall MI with RV INFARCT
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Decreased preload will cause sudden hypotension and
increase infarct size
These patients need fluids to increase preload and
help fill the malfunctioning/weakened ventricle
Treatment in the ED: USA/NSTEMI
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Basically the same, but without the cath
lab or fibrinolytics
IV, O2, monitor
ASA, heparin, NTG, ? beta blocker,
morphine
Plavix and GIIb/IIIa inhibitors potentially
after discussion with cardiology
Admit to a monitored unit
Chest Pain: low risk, but risky enough
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Patients who are low risk with risk factors
(silly isn’t it?), chest pain free, and have a
normal ECG and enzymes
Observation unit for serial cardiac enzymes
and ECG
Stress test vs. CTA
Cardiology consult variable
Chest Pain: What is it?
38 y/o female presents with sudden onset of
chest pain and shortness of breath after
retrieving her bags at the baggage claim
from a flight home from Hawaii. She
states that it is worse when she takes a
deep breath. She also complains of this
aching pain in her right leg when walking.
Chest Pain: What is it?
80 y/o bedridden patient sent from the NH with
mental status changes and hemoptysis. She is
pleasant during the conversation, but has no idea
why she is here. She is actively coughing and
appears to have increased work of breathing.
PMHx: positive for almost everything (she is 80)
Vitals: HR 110, BP 90/60, RR 28, sPO2 88% RA
Lungs: bibasilar rales with right mid lung rhonchi
Pulmonary Embolism – 2006 Stats
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Approximately 1 in every 500-1000 EC
patients has a PE
EM MDs correctly diagnose about 50%
10% of EC patients with PE die within 30
days even when PE is promptly diagnosed
and treated
PE – Risk Factors
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Carcinoma
Immobility
Trauma or surgery in the last 4 weeks
Smoking
Estrogen/OCP
Pregnancy/PP
Thrombophilia
Connective Tissue Dz
Prior PE or DVT
PE – Signs and Symptoms
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Chest Pain
Dyspnea
Hemoptysis
Splinting
Syncope
HR > 100
Pulse ox < 95%
Unilateral arm or leg swelling
PE – Diagnosis
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Basic Labs – CBC and Chem 7
? Labs – CK-MB, troponin, PT/PTT
D-dimer – low risk patients only with low
pretest probability
CXR
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Exclude other diagnosis – CHF, PNA, PTX
Unilateral basilar atelectasis increases the
probability of PE
Hamptom’s hump – wedge shaped infarction
Westermark’s sign – unilateral lung oligemia
PE – Hampton’s Hump
PE – Westermark’s Sign
PE – Diagnosis
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ECG
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Again to exclude other diagnosis
Most common finding is sinus tachycardia
T wave inversions V1-V4
McGinn-White Pattern – S1Q3T3
New incomplete or complete RBBB
Chest CT – moderate to high risk patients or
pre-test probability, positive D-dimer
PE – ECG
PE – ECG
PE – Treatment
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Heparin unfractionated 80 U/kg bolus then
18 U/kg/hr
LMWH 1 mg/kg SQ q12 hours
Coumadin – usually started on the floor
PE – Treatment
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IVC filter – for pts who failed
anticoagulation or have contraindications
Thrombolytics – consider in high risk pts
such as systolic hypotension, persistent
hypoxemia, elevated troponin or BNP
(early shock or shock)
Surgery – large clot burden, refractory
hypotension, floating emboli in the R heart
Chest Pain: What is it?
18 y/o tall, thin healthy male c/o sudden
onset L sided CP with shortness of breath.
The pain started while he was inhaling on a
marijuana cigarette. It hurts more to
breathe.
Vitals: HR 110, RR 28, BP 110/70, sPO2 96%
Chest Pain: What is it?
60 y/o male with a history of severe COPD c/o
increasing shortness of today that is not relieved
with his home inhalers.
Vitals: HR 110, RR 28, BP 110/70, sPO2 90%
Heart: distant, tachycardic and regular
Lungs: diffuse wheezing, decreased breath sounds
on the right
Pneumothorax
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Primary Spontaneous – occurs in people
without clinically apparent lung disease
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More common in men
Associated factors = tall, smoking, changes in
ambient atmospheric pressure, genetics, MVP,
Marfan’s syndrome
Disruption of the alveolar-pleural barrier is
thought to occur when a bleb or bulla ruptures
into the pleural space
Pneumothorax
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Secondary Spontaneous – occur with
known underlying pulmonary disease
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More common in men
Associated with any underlying pulmonary
disease including infection, ILD, neoplasms,
COPD, asthma, etc…
Weakening of the alveolar-pleural barrier
occurs secondary to the underlying lung
disease either from inflammation or
development of bullae
Pneumothorax
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Iatrogenic
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Complication of intubation or aggressive BVM,
central line placement, or any endoscopic
procedure involving the trachea or esophagus
Consider in any stable patient with acute
deterioration, hypoxia, or increased difficulty
with ventilation
Tension Pneumothorax
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Positive intrapleural pressure causes
compression of the mediastinum and the
contralateral lung
Pressure exceeding 15 to 20 mm Hg
impairs venous return to the heart
Leads to cardiovascular collapse if not
treated immediately  this is a clinical
diagnosis not a radiographic one!
Pneumothorax – Symptoms
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Ipsilateral sharp CP
Dyspnea
Pleuritic pain
Cough
Pneumothorax – Signs
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Sinus tachycardia
Hyperresonance
Decreased breath sounds
Unilateral enlargement of the hemithorax
Splinting
Hypoxia
Pneumothorax: Diagnosis
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Clinically for tension PTX
CXR
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Radiolucent band devoid of lung markings
Inspiratory/expiratory views
Lateral decubitus views in sick patients
Supine CXR may have deep sulcus sign
Thoracic ultrasound
Chest CT
Pneumothorax - Tension
Pneumothorax – Deep Sulcus Sign
Pneumothorax: Management
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Tension – needle decompression
Tube thoracostomy  20-28 F for air, 32F
at least if fluid is present
Observation – for PTX < 20% collapse
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Reabsorption Rate
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1-2% per day
4-8% if on 100% NRB
Chest Pain: What is it?
60 y/o male complains of sudden onset
tearing chest pain that went up into his jaw,
through to his back, and then down into his
abdomen. He also vomited once, is
diaphoretic, and appears very anxious.
Vitals: BP 190/120, HR 110, RR 22, sPO2 95%
Aortic Dissection
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Occurs more often in men older than 40
HTN is the most common risk factor
Associated with cardiac surgery, bicuspid
aortic valve, stimulant use, and trauma
Age<40, associated with congenital heart
disease, Marfan, Ehlers-Danlos, and giant
cell arteritis
44% of pts with Marfan’s will develop an
aortic dissection
Aortic Dissection
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Type A – 62%
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Involve the ascending
aorta  more lethal
Type B – 38%
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Do not involve the
ascending aorta
Pt more likely to be
older, smoke, have
chronic lung disease,
HTN, or atherosclerosis
Aortic Dissection - Diagnosis
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Labs – CBC, chem7, PT/PTT, type & cross,
CK-MB, troponin
ECG – exclude other dx, 15% may have
ischemic changes  3% dissect back and
most commonly involve the RCA, may have
LVH or nonspecific ST or T wave changes
CXR – abnormal in 80% but nonspecific
findings
Aortic Dissection - Diagnosis
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CT scan – test of choice
TEE – limited by availability and operator
Aortography – no longer the test of choice
MRI – excellent test but limited by
availability and instability of the patient
Aortic Dissection - Management
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Opioids – decrease pain and sympathetic
tone
Beta blockers – esmolol and labetalol
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Decrease BP and HR to decrease shearing forces
Should be started first unless the pt is bradycardic
Nipride – vasodilator, used in conjunction
with a beta blocker to maintain SBP 100120
Aortic Dissection - Management
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Hypotensive pts – measure BP in all 4
extremities to make sure it is real, IVF,
blood, immediately to OR
Type A  OR (27% mortality if treated
surgically vs. 56% if treated medically)
Type B uncomplicated – 10% mortality
when treated medically (32% mortality if
complicated)
Chest Pain – What is it?
22 y/o healthy male complains of chest and back
pain after forcing himself to vomit. He states he
had food stuck in his chest while eating at
Mongolian BBQ and then forced himself to vomit
for relief. He now says that his voice is hoarse, it
hurts to breathe deep, and he is still very
nauseated. He tried to drink some water, but
this only intensified the pain.
Vitals: HR 120 BP, 130/90, RR 25, sPO2 97%
Esophageal Rupture – Boerhaave’s
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15% are spontaneous with the remainder
being iatrogenic from endoscopy, NGT, ETT,
combitube, foreign body…
90% of spontaneous ruptures occur in the
distal esophagus
DX – CXR, gastrograffin swallow, CT
Management
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IV antibiotics
NPO and likely NGT
Surgery consult
Chest Pain: What is it?
26 y/o male c/o retrosternal, sharp CP, difficulty breathing,
pain when breathing deeply, and worsening dyspnea
tonight when he laid down to sleep. He states that for the
last week he has had URI symptoms and low grade fever,
but now feels that it has moved into his chest with the
increasing pain and difficulty breathing.
Vitals: HR 110, BP 110/80, RR 24, sPO2 98%
Heart: Tachycardic and regular, (+) pericardial rub
Lungs: CTA
Bedside TTE is negative for effusion
Pericarditis
Pericarditis
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Causes – infectious, injury/trauma,
metabolic, systemic (RA), carcinoma, or
aortic dissection
DX – clinical suspicion, ECG, echo
Echo – pericardial effusion and tamponade
are worrisome complications  pts should
be put in obs or hospitalized
Treatment – NSAIDS, steroids for pts who
cannot tolerate NSAIDS
THE END!