quiz 1 - chest pain 1 Flashcards
pathophysiology to chest pain
-Visceral pain
-Internal organs
-Difficult to describe or localize
-Often referred to adjacent somatic nerves
-Somatic pain
-Sharp and well localized
what affects pain perceptions
-Age (elderly)
-Sex (female)
-Comorbidities (diabetics)
-Medications
-Drugs
-Alcohol
-Psychological factors (psychiatric illness, AMS, low IQ)
-Cultural factors
Why is it important to know these? -> 2x higher mortality
-elderly, females, DM -> atypical sx
initial actions and primary survey in chest pain
-“Sick vs. Not sick”
-Primary survey: ABCs and vital signs
-!Obtain an ECG < 10 minutes!
-Team work:
-Cardiac monitoring & IV access
-Defib pads, airway cart
-Focused history & exam
-OLDCAAART
-over a few minutes - 30 mins -> more likely ACS
-sudden onset, or lasting 5 days -> maybe something else
-Assess for cardiac risk factors
-Assess for life-threatening causes -> Look for: Surgical scars, Chest wall deformities
-Other rapid diagnostics
-ALL CHEST PAIN GETS A CXR AND ECG MINIMUM
chest pain: differentials of consequence
-LIFE THREATENING (6 you cant miss)
-ACS
-PE
-dissestion
-tension ptx
-tamponade
-esophageal rupture
-POTENTIAL MORTALITY (can work it up typically)
-simple ptx
-peri/myo/endocarditis
-pneumonia
-aortic stenosis
-perforated ulcer*
-pancreatitis/cholecystitis
-heart failure
-BENIGN (Dx of exclusion)
-anxiety
-costochronditis
-esophagitis
-gastritis
PE for chest pain (didnt go over really- vitals, legs, skin)
-VITALS
-Hypotension -> Obstruction: Tension PTX, Tamponade, PE
-Hypoxemia -> Tension PTX, CHF, PE
-Tachycardia/Tachypnea -> Non specific
-Pulsus paradoxus: Tamponade
-CARDIAC EXAM
-Diminished or muffled heart sounds -> Pericarditis or tamponade
-Diastolic murmur -> Aortic regurgitation, TAD, endocarditis, myopericardial syndromes
-S3 gallop -> Heart failure
-Extremities:
-Pulse deficit
-Asymmetric leg swelling !!
-Peripheral edema !!
-NECK:
-JVD -> tamponade, PE, tension PTX, heart failure
-PULM EXAM
-Absent breath sounds -> PTX
-Wheezing -> COPD/Asthma, PE (60%), pneumonia
-Wet crackles -> CHF
-CHEST WALL
-Subcutaneous emphysema -> esophageal perforation
-Pain reproduced with palpation -> decreases chance of ACS
-ABDOMEN
-Epigastric tenderness -> abdominal OR inferior MI
Pulsatile abdominal mass -> AAA
-SKIN!!
-Zoster
-IVDU
-Trauma
-NEURO
-Focal neuro deficits:
-Dissection or embolization into cerebral vessels or spinal cord
initial orders in chest pain
-Vitals signs and pulse ox
-Cardiac monitor
-Peripheral IV line
-Oxygen if hypoxic (<92%)
-Consider placing defib pads
-ECG (stat <10 min)
-CXR 1-view STAT
-Labs as indicated : CBC, CMP, Trop q3h x 3, BNP
-ASA chewable 325mg (not if AAD suspected)
-Nitroglycerin sublingual 0.4, repeat x3 q5 min if needed, hold for hypotension / recent sildenafil use
tx of life threatening causes of chest pain
-ACE/STEMI
-ED -> ASA, nitroglycerin (if no CI), heparin, dual antiplatelet therapy
-def tx -> PCI with stenting or CABG
-PE
-ED -> heparin/Lovenox/DOACs or TPA
-def tx -> anticoagulation, thrombolysis, embolectomy
-AORTIC DISSECTION
-ED -> pain control, BP control
-def tx -> surgery for type A, medical management for type B
-TENSION PNEUMO
-ED -> needle decompression/chest tube
-Def tx -> chest tube management, pleurodesis
-ESOPHAGEAL RUPTURE
-ED -> IV antibiotics, NPO, PPI
-Def tx -> surgical intervention/ICU care
-PERICARDITIS/TAMPONADE
-ED -> IVF, US guided pericardiocentesis
-Def tx -> cath lab for drain placement versus pericardial window
test yourself
-Chest pain, weakness, nausea, fatigue, diaphoretic -> MI
-Pleuritic chest pain, sob, recent orthopedic surgery -> PE
-Burning, gnawing chest pain with brackish acidic taste in the back of the mouth -> GERD
-Chest pain + cocaine use, ripping, severe, back pain, paresthesia’s -> dissection
-Chest pain, fever, cough, sputum and rales -> pneumonia
-Sudden chest pain with crepitus after vomiting -> esophageal rupture (subq air)
-Sudden onset pleuritic sharp chest pain, sob and decrease breath sounds on one side -> pneumothorax
-Sharp constant chest pain worsened by lying flat -> pericarditis
-Sharp chest pain and palpitations with mid systolic click -> mitral valve prolapse
dispositions
-ICU
-hemodynamically untable
-massive PE
-STEMI
-aortic dissections, tamponades, mediastinitis
-FLOOR/WARDS
-NSTE-ACS and PE cases with RV dysfunction
-OBSERVATION
-non low risk ACS with neg troponins and non specific ECGs
-high risk pneumonias
-unstable angina
-simple pneumothoraxes s/p procedure
-OR
-esophageal rupture
-aortic dissection type A
-HOME
-stable angina
-low risk of ACS (HEART score <3)
-low risk of PE (PERC neg)
-reliable PE pts (PESI low)
-GERD, MSK, other low risk dx
A 32-year-old woman with chest pain, sweating, vomiting presents…
Triage nurse wrote “just anxious” and placed her in the waiting room
History: Onset 30 minutes ago. Associated with diaphoresis, vomiting which has resolved. Pain is present but improved. Radiates to both arms.
Family history: early MI
The ECG showed ST depression in leads I and aVL
Not diagnostic of STEMI
Based on your clinical concern, you asked for the patient to be placed in the critical care room
You ask for serial ECG q10 minutes, and defibrillator pads to be placed
Triage nurse wrote “just anxious” and placed her in the waiting room
History: Onset 30 minutes ago. Associated with diaphoresis, vomiting which has resolved. Pain is present but improved. Radiates to both arms.
Family history: early MI
The ECG showed ST depression in leads I and aVL
Not diagnostic of STEMI
Based on your clinical concern, you asked for the patient to be placed in the critical care room
You ask for serial ECG q10 minutes, and defibrillator pads to be placed
Ordered:
325 mg of aspirin PO
0.4 mg of nitroglycerin SL since her BP was OK
The second ECG was obtained, and it showed >1 mm of ST elevation in leads II and aVF.
You activated the cardiac catheterization lab and discussed your findings with the interventional cardiologist.
The cardiologist could not see the ECG in real-time and was reluctant to take her for catheterization because of her age.
You went to reassure the patient and discuss the plan, but as you walked into the room, she became unresponsive, and you noted ventricular fibrillation on the monitor.
You quickly charged the defibrillator and delivered a single shock. The patient was in VF for a matter of seconds, and regained a pulse and consciousness after defibrillation.
The patient was quickly taken to the cardiac catheterization laboratory.
-DYNAMIC ECG CHANGES
-RADTION OF PAIN
acute coronary syndrome
->8 mil visits to ED each year with potential acute heart disease
-15% will have ACS
-ACS is assoc with high mortality
-know the photo
unstable angina vs NSTEMI vs STEMI
ACS risk factors
->40 yo
-Male or Post-menopausal female
-Atherosclerotic disease risk factors:
-Known CAD
-HTN
-Hypercholesterolemia
-Diabetes
-Vascular disease
-Tobacco use
-Truncal obesity
-Cocaine/amphetamine use
-Family history
-Sedentary lifestyle
-HIV + HAART
-Other: Lupus, CKD, Alcoholism
non-atherosclerotic causes of MI
-normal stress test
-Less common
-Emboli (valve, PFO)
-Coronary occlusion secondary to vasculitis
-Primary coronary vasospasm (cocaine)
-Spontaneous coronary dissection
-Aortic dissection
-Other factors leading to mismatch of oxygen supply and demand (example: significant GI bleed)
presentation of ACS
-CLASSIC
-Frequently begin at rest
-Retrosternal / substernal
-Crushing, squeezing, tightness, pressure, discomfort
-!!Exertional chest pain
->2 minutes, as long as 30 minutes
-!!Radiation (arms, neck, jaw)
-Associated with diaphoresis!, dyspnea, !nausea, vomiting!, pallor, fatigue (esp in elderly)
-!!similar to past and proven infarcts
-NON-CLASSIC /ATYPICAL
-These are still common!
-Chest pain lasting for a few seconds
-Chest pain constant for 12-24 hours
-Chest pain worsened with body movements and position
-Stabbing, well-localized, position, pleuritic -> uncommon but does not exclude
anginal equivalents: do not have to be associated with chest pain
-Dyspnea (at rest or exertion)
-Diaphoresis
-Nausea
-Lightheadedness
-Generalized weakness
-Acute changes in mental status
-Shoulder, arm!, jaw discomfort
-Epigastric or upper abdominal discomfort -> Especially in inferior wall ischemia
-Palpitations
-can be MIs with just one symptom
pt arrives with chest pain suggestive of ischemia (not on pp?)
-door to ECG -> done and read within 10 mins
-EMERGENT CARE
-IV access x2
-cardiac monitoring
-O2 (if <90%)
-ASA 162-325mg chewed
-nitro 0.4mg SL (if no CI)
-+/- plavix
-+/- morphine
-INITIAL LABS AND TESTS
-ECG (serial)
-stat CXR
-cardiac enzymes (serial)
-troponin*, CBC, CMP, coags, BNP, T&S
-HX AND PE
-primary survey -> initial exam of neck (for distended neck veins), heart, lungs, abdomen (for enlargement of the liver or spleen), and extremity examination for circulation and edema
-Assess eligibility for reperfusion
-± POCUS
-ACC/AHA guidelines: Door-to-ECG within 10 minutes, Biomarkers in 30 minutes, PCI in 90 minutes
coronary arteries anatomy
ECG leads -> arteries
evolving MI
-normal -> MI -> hyperacute t waves (wide, tall, symmetrical) -> hours to days -> ST elevations and T waves -> Q waves -> after a few weeks -> ST elevation improves
ischemia ECG
-ST depressions
-Horizontal or down-sloping ST segment depression with or without T wave inversion (TWI)
-The ST depression is typically symmetrical
-anterior ischemia- pic
t wave inversions (TWI)
-inferior t wave inversion due to acute ischemia (L)
-t waves can persist for the rest of a pts life after a MI
-lead 3 can have isolated t wave inversion -> normal
-inferior t wave inversion with Q waves - prior myocardial infarction (R)
NSTEMI ECG
ST depressions
-lateral, anterior
hyperacute t waves
-STEMI early on
-large, symmetrical
-could also be hyperkalemia- DKA
-can look like early repolariztion
STEMI criteria
-NEW ST segment elevation ≥1mm in ≥2 contiguous leads
-Except in V2-V3 (see below)
-NEW ST segment elevations in V2-V3 meeting these criteria:
-≥ 2.5 mm in men aged < 40 years
-≥ 2 mm in men aged > 40 years
-≥ 1.5 mm in women
-these are more bc they are physically closer to the chest wall and naturally have a higher voltage
-Reciprocal changes (ST depression in opposite leads)
-Not ALL STEMI show reciprocal changes, usually signifies very large STEMI
STEMI ACUTE ANTERIOR INFARCT
-anterior septal MI
-V4- tombstones
STEMI LATERAL WALL
-left circumflex artery
-reciprocal changes in 2,3,aVF -> confirms the STEMI
-STEMI INFERIOR WALL
-affects the RV -> hypotensive -> DONT GIVE NITRO
-the heart will get no fluid
-Often associated with N/V, bradycardia!
-RCA often supplies the SA/AV node
-Increased vagal tone
-Hypotension can occur with RV infarct
-Increase preload with IVF
-Avoid nitrates
right ventricular infarct
-preload dependent = tx with IV fluids
-nitrates are contraindicated
-some do a right sided ECG -> flip it
A 74-year-old woman with chest pain is delivered to your ED by EMS…
-Paramedics state they have given her 324 mg of aspirin orally and 3 doses of 0.4 mg of nitroglycerin sublingually.
The patient’s pain improved, but is still present.
Her vital signs are normal.
The paramedic hands you an ECG that he obtained and states that there is anterior ST-segment depression concerning for ischemia, but no ST elevation.
You look at the tracing and note ST depression in leads V2and V3. You wonder whether this could actually be a STEMI, and what would be the best way to confirm your suspicion…
-Paramedics state they have given her 324 mg of aspirin orally and 3 doses of 0.4 mg of nitroglycerin sublingually.
The patient’s pain improved, but is still present.
Her vital signs are normal.
The paramedic hands you an ECG that he obtained and states that there is anterior ST-segment depression concerning for ischemia, but no ST elevation.
You look at the tracing and note ST depression in leads V2and V3. You wonder whether this could actually be a STEMI, and what would be the best way to confirm your suspicion…
You noticed ST depression in leads V2and V3, with a prominent R wave and upright T wave.
Based on this, you obtained posterior leads, V7, V8, and V9. The posterior tracing (V7, V8, V9) showed ST elevation of 1 mm in leads V7and V8.
You promptly activated your cardiac catheterization lab and spoke with interventional cardiology. The patient had been given aspirin in the field. You administered nitroglycerin and prepared the patient for transfer to the catheterization lab. About an hour later, the interventional cardiologist called and informed you that the patient had a 99% circumflex artery occlusion that required a stent. The patient was now in the ICU and doing very well.
You successfully diagnosed an isolated posterior (inferobasilar) STEMI.
stemi posterior wall
-aka inferobasal stemi
-infer you are seeing the a posterior MI when you see reciprocals
-V1 and V2 depression
posterior MIs
-Rare (3% of MI)
->2 mm STD in V1-V4
-Tall R waves (R:S >1)
-!Associated with inferior MIs
-!Which can cause RV dysfunction
-Caution with nitrates
-Fluid challenge if hypotensive
-Acute RV failure -> JVD
-Lung sounds should be clear in these patients
other ECG findings to treat similar to STEMI
-these are complete occlusions -> BAD
-DeWinter T-waves
-Isolated ST elevation in aVR with upsloping ST depressions in precordial leads
-LAD occlusion
-isolated ST elevation in AVR
-upsloping ST in the precordial leads
-completely occlusive LAD
-call cardiac cath
-LBBB showing a STEMI equivalent via Modified Sgarbossa criteria
-Wellens
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STEMI in AVR (De winter)
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wellens pattern
-strongly assoc with LAD occlusions !!!!
-deep wide symmetrical t wave inversion in the precordial leads
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-left bundle branch block
-how do you know this isnt a STEMI -> you dont -> look at criteria
normal LBBB
-QRS > 120ms
-V1 will have dominant S waves
-Lateral lead R waves may be either “M” shaped, notched, monophasic or RS complex
-!Normal LBBB will have “discordance”
-(The T wave goes in the opposite direction of the QRS complex)
-NORMAL- positive deflection depolarization -> negative repolarization (vice versa)
-NORMAL LBBB
-QRS duration > 120ms (wide>3 small boxes)
-Broad-notched or monophasic R wave in I, aVL, V5, V6
-Absent Q V6
-Associated with a variety of cardiac comorbidities
-Discordant: ST and T are in opposite deflection: ST segment-T wave V1-V3
-R-S or Q-S pattern in V1-V3
sgarbossa’s criteria
-In patients with LEFT BUNDLE BRANCH BLOCK (LBBB) or VENTRICULAR PACED RHYTHYM, it can be difficult to diagnose an infarct (because T-wave inversions are expected).
-The Sgarbossa criteria can help diagnose infarction in the setting of LBBB
-dont memorize it
-if any one it met -> MI
example of sgarbossa rule
-ischemia- + QRS and positive ST segement elevation -> going the same way
-A. more than 25% -> ischemic
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-criteria 1 -> no
-criteria 2 -> V2 and V3 -> concordanant ST depression YES
-this is ventricular paced with ischemia
differentials for ST segment elevation (went over quick)
-STEMI ->
-Chest pain, dyspnea, diaphoresis, anginal equivalents
-ST elevation in anatomically contiguous leads with reciprocal ECG changes
-PERICARDITIS ->
-Pleuritic pain that may improve with sitting up down worse with lying down
-Diffuse ST segment elevation with concave morphology
-No ST depression or reciprocal changes
-MYOCARDITIS ->
-ST segment changes may resemble acute ishcemia
-ELECTROLYTE RERANGEMENT (HYPERKALEMIA) ->
-tall symmetric peaked T waves may mimic ischemia
-LBBB PATTERN ->
-appropriate discordant ST segment elevation typically seen in V1-V3
-BRUGADA ->
-ST elevation >2mm in >1 of V1-V3 followed by neg T wave
-HYPOTHERMIA (OSBORN WAVE) ->
-positive deflection at J wave, core temp <30c
-BENINGN EARLY REPOLARIZATION ->
-asymptomatic, young, notching at J point
myocardial markers
-Troponin (I&T): are exclusive to myocardial cells but can leak out for a variety of reasons (not just ischemia)
-Degree of myocardial damage & mortality is correlated with the degree of troponin elevation.
-Troponins in ischemia will rise around 3 hrs after injury -> Often recheck at 3 and 6 hours
-Ultra-high sensitivity troponins are 1,000-10,000x more sensitive
-there is no longer a role for CK-MB, LDH, or other cardiac markers for ACS
-!CK-MB: an early marker for myocardial necrosis
-Myoglobin: an early marker for muscle injury -> Non-specific, not ordered commonly
non-MI causes of troponin elevations
-Tachycardia (24%)
-Myocarditis (16%)
-Congestive heart failure*
-PE
-Electrical injury
-Chest contusion
-Stroke
-Sepsis
-Collagen vascular diseases
-GI bleeds
-Diabetic ketoacidosis
-COPD exacerbation
-Renal failure- dont clear troponins as well (that are normally released)
-Cardiomyopathy
-Post-coronary artery bypass
-ROSC after cardiac arrest
-CO poisoning
-Pancreatitis
-Hypoxia / hypercarbia
-Demand ischemias!
MONA
DONT USE
-morphine masks pain
-O2 only if needed
-Nitrates arent given in RV or inferior MI
-aspirin is good
what to give during AMI
-ABCs
-IV access
-Cardiac monitoring
-Anti-ischemic therapies
-Supplemental oxygen if SpO2 <90%
-Nitroglycerin**: coronary vasodilator, ↓ preload
-Avoid w/ recent sildenafil in past 24-48 hours
-Caution in inferior MI, aortic stenosis, hypotension
-0.4 mg sublingually every 5 minutes for 3 doses
-nitro relief does not dx ACS -> it also relieves GERD bc it relaxes the LES
-NOTE: Morphine for analgesia only when maximal anti-ischemic therapy is ineffective for alleviating angina
-antiplatelets (cont.)
-anticoagulants (dont need to know details)
-LMWH/UFH- controversial, follow hospital protocol
-STEMI getting PCI: UFH 70-100U/kg IV bolus
-STEMI getting fibrinolysis: LMWH, UFH, Fondaparinux are all acceptable, 48 hours minimum
-Other consideration- start these but not in the ER
-Beta blockers:
-↓CP, ↓stress of myocardium, ↓size of infarct
-Metoprolol 5mg IV doses q5 min x 3 doses or 50mg PO
-Not commonly started in ED
-Statins:
-Start within 24 hours
-Not commonly started in ED
anti-platelet therapy: AMI
-!Aspirin 162-325mg chewed** -> Reduces mortality by 23%
-P2Y12 inhibitor:
-Can be given ASAP or at the time of PCI; institution based
-Clopidogrel (Plavix)
-ASA+ clopidogrel has been shown to further reduce the risk of MACE in patients with NSTEMI
-Loading dose for STEMI 600mg vs UA/NSTEMI 300mg
-Ticagrelor (Brilinta)
-?better than clopidogrel, though it has a higher chance of bleeding
-Loading dose 180mg- for NSTEMI and STEMI
-Prasugrel (Effient) at 60mg loading dose
reperfusion therapies for STEMI
-Tick tick tick!
-!!Percutaneous cardiac intervention (PCI) within 90 minutes
-DOOR-TO-BALLOON 90 minutes per AHA (120 for non-PCI facilities)
-Symptoms <12 hours, Symptoms 12-24 hours with ongoing ischemia, or if signs of cardiogenic shock and severe acute heart failure regardless of time
-!!Thrombolytic treatment within 30 minutes of arrival
-DOOR-TO-NEEDLE 30 minutes per AHA
-Inferior to PCI but more readily available
-Best reduction in M&M if done within 12 hours of symptom onset
-4 agents: Tenecteplase (tPA), reteplase, alteplase
-Transfer to PCI facility after beginning fibrinolytics!!!!
STEMI cardiac care: perfusion therapy options indications
-thrombolysis indications:
-door to needle 30 mins
-Chest pain <12 hrs
-Unrelieved with nitrates
-PCI is not available or delayed
-Still go to PCI after thrombolysis
-PCI preferred if:
-door to balloon <90 mins -> extend up to <120 if transfer
-PCI is ALWAYS THE PREFERRED CHOICE IF AVAILABLE
-Concurrent pulmonary edema, cardiogenic shock, or severe acute heart failure regardless of onset of symptoms
-STEMI diagnosis in doubt
tPA contraindications (dont memorize?)
-ABSOLUTE
-PCI immediately available
-History of !intracranial hemorrhage!
-Known !intracranial neoplasm or vascular lesions!
-Intracranial or intraspinal surgery within !3 months!
-Active internal bleeding (except menses) or known bleeding disorder
-!Embolic stroke within 3 months! (exception: embolic stroke within 3 hours)
-Suspected !aortic dissection!
-Significant facial or head trauma within !3 months!
-RELATIVE
-Uncontrolled severe hypertension(>180 systolic, >110 diastolic)!!!
-Prolonged cardiopulmonary resuscitation (>10minutes) or recent surgery (<3 weeks) or non-compressible vascular puncture
-Recent internal bleeding or active peptic ulcer disease
-Pregnancy
-Current anticoagulation with high international normalized ratio (INR)
-For streptokinase: prior exposure to the drug or history of allergic reaction
cocaine associated STEMI
-Cocaine causes vascular change and alteration in platelet function and coagulation
-Similar management to normal STEMI -> Still send to PCI > fibrinolysis
-!!Benzodiazepines for chest pain, sedation, decreased HR/BP
-No beta blockers -> unopposed alpha receptor stimulation
special considerations
-Don’t let age fool you!
-!Relief with a “GI cocktail” does not exclude ACS- famotidine, lidocaine, etc.
-!Lack off relief with nitroglycerin does not exclude ACS
-Lack of risk factors does NOT preclude ACS
-Commonly acknowledged risk factors to ask about:
-HTN, HLD, DM
-Cigarette use
-Older age
-Family history of ACS/STROKE
-Sedentary lifestyle
-Cocaine or similar drug use
people we arnt sure about:
36yoF presents with sharp CP this AM while at rest
Nausea, vomited x 1
Became dizzy, diaphoretic
No radiation of pain
No SOB
Few episodes over the past 2 days, now asymptomatic
Smokes ½ PPD, no other cardiac risk factors
PE: 150/90 mmHg, otherwise normal exam
ECG: Non specific changes
36yoF presents with sharp CP this AM while at rest
Nausea, vomited x 1
Became dizzy, diaphoretic
No radiation of pain
No SOB
Few episodes over the past 2 days, now asymptomatic
Smokes ½ PPD, no other cardiac risk factors
PE: 150/90 mmHg, otherwise normal exam
ECG: Non specific changes
risk stratification: HEART score
risk stratification: HEART SCORE (dont memorize the score)
-Most sensitive test for 30-day MACE in undifferentiated chest pain
-MACE (major adverse cardiac event) is defined as death, non-fatal myocardial infarction (MI), or revascularization procedure within a !6-week period!
-Distinguish low-risk from high-risk chance of risk MACE -> Can I discharge, observe or admit?
-Score 0-3 is <2% risk of MACE - discharge
-good candidate for discharge with outpt eval within 1-2 weeks
-Score 4-6 is 5-20% risk of MACE - stress
-based on a single troponin
-inpt hospitalization vs. expedited outpt evaluation
-Score ≥7 is 50-72% risk of MACE –> admit
-*Risk factors: HTN, HLD, DM, smoking, family history, and obesity
Risk stratification for STEMI and NSTEMI in ED
management of NSTEMI in ED
take home points for chest pain risk stratification
-Make sure to get a GOOD history (OLDCART)
-Document the history well
-Document your accelerated diagnostic protocol score (HEART score)
-If clinical evaluation suggests higher risk, THEN send for further testing
risk management
-“The patient with chest pain was young, so I didn’t get an ECG.”
-“The patient had nausea and diaphoresis, but he didn’t have chest pain, so I didn’t get an ECG.”
-“The patient had shortness of breath and cough without chest pain, so an ECG was not obtained in triage.”
-“I didn’t get another ECG, since the first one looked normal.”
-“I identified STEMI, but a serum troponin resulted negative before the patient went to the catheterization lab. Based on the troponin, I canceled the catheterization lab activation.” STEMI is an ECG diagnosis!
Which of the following pericardial complications can occur more than 2 weeks after a myocardial infarction?
Peri-infarction pericarditis
Pericardial effusion due to myocardial rupture
-Dressler syndrome (post cardiac injury syndrome)!!!!!!!!!!!
Pericardial tamponade
Fibrinous pericarditis
39M h/o HTN (non-adherent with HTN meds due to insurance issues for 5 days), renal colic, back pain c/o sudden onset left upper back pain, non-radiating, unable to get comfortable and feels something moving in his abdomen. Pt states that he experienced sudden onset of a similar left sided upper back pain that lasted for 20 minutes earlier this week but resolved spontaneously. Notes that he has never had pain this bad, so he came to the ED. Tried Motrin, anti-gas meds, and heat without resolution.
BP:173/94 | Pulse:84 | Resp:18 | Temp: | SpO2:97%
General- Alert and oriented, NAD
HEENT – N/A
Neck - Supple, no stridor
Chest - clear, good excursions
Cardiac - S1, S2 regular, no MRG
Abd - soft, bs wnl, no organomegaly, no masses, non-tender, no guarding, no rebound
Back - no reproducible tenderness, no cvat
Ext - no edema, non-tender, good perfusion
Neuro - awake, alert, non-focal
BP:173/94 | Pulse:84 | Resp:18 | Temp: | SpO2:97%
General- Alert and oriented, NAD
HEENT – N/A
Neck - Supple, no stridor
Chest - clear, good excursions
Cardiac - S1, S2 regular, no MRG
Back - no reproducible tenderness, no cvat
Ext - no edema, non-tender, good perfusion
Neuro - awake, alert, non-focal
Based on my current evaluation, it is my medical judgement that this patient has poorly controlled bp and upper back pain.
Plan:
Labs
EKG
CXR
CT chest
Pain meds
Cardiac monitor
Follow
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type A dissection extending into the aortic bifurcation
thoracic aortic dissection
-A rare, deadly, and confounding diagnosis
-~40% are initially missed
-Mortality is 40% in acute phase, 70% in two weeks
stats on aortic dissection
-3 out of 1,000 chest / back / abdominal complaints
-1 AAD for every 80 MI case
-Mean age is 62
-Rare under 40
-Bicuspid aortic valve
-Aortic aneurysm
-Connective tissue diseases
-Tertiary syphilis
-Cocaine use
-Family history matters
-Risk factors:
-Hypertension (72%)
-Atherosclerosis (30%)
-Connective tissue disorder (5%)
-Pregnancy
aortic dissection pathophys
-Tear of intima (most inner), into the media (the elastic middle)
-False lumen forms
-Increase in spread of the false lumen with each pump of the heart -> RATE CONTROL under 60 bpm super important
-High blood pressure
-High heart rate
MC sx in AD
-Any pain (96%)
-!Severe/worst pain (91%)
-Abrupt onset (87%)
-!Chest pain (76%)
-Widened mediastinum (60%)
-Back pain (54%)
-!Tearing/ripping (51%)
-Aortic insufficiency murmur (32%)
-!Pulse deficit (15-28%)
-Non-diagnostic CXR (33%)
-syncope -> dissect all the way back to the heart -> Tamponade -> faint
AD: CXR
-Normal in 5 out of 6 dissections
-Findings are often non-specific
-!“Widened mediastinum” is subjective
-Pleural effusion
-Must do a CT angiography if concerned!
-IV contrast
-MRI: Is this available and close?
-TEE: difficult to obtain
-TTE: often not sensitive enough
jkdsnaf
CT of AD
pathophysiological consequences of AAD
-Ascending aorta -> Hemopericardium (syncope, sudden death)
-Ascending or descending -> Hemithorax (sudden death)
-Abdominal aorta -> Retroperitoneal hemorrhage (back pain+shock)
-Abdominal aorta -> Intraperitoneal hemorrhage (rarer, acute abd)
-Coronary vessels -> STEMI
-Common carotids -> Stroke
-Subclavian -> Upper limb ischemia
-Mesenteric vessels -> Ischemic bowel
-Renal vessels -> Hematuria *
-Spinal artery -> Sudden paraplegia
-PERICARDIAL TAMPONADE IS MCC OF DEATH IN THESE PTS
AAD management
-Definitive management depends on type of dissection
-Stanford A - Emergency SURGERY (CT surgery)
-Stanford B - Endovascular stenting and Medical management
-Anticoagulation and fibrinolysis = bad!
BP/HR goals in AAD
-!GOAL: HR < 60 & SBP <120
-HR is more important -> every beat pumps more blood into it
-IV agents
-!!First line: BETA BLOKCERS!!!!!
-!Esmolol 50 mcg/kg/min IV
-Labetolol 20mg IV (onset 5-10 minutes, duration 3-6 hours)
-Nicardipine 5mg/hr IV
-Vasodilators (second line, after beta blocker)
-Nitroprusside 0.25mcg/kg/min IV
-No nitrates by themselves! Reflex tachycardia
AAD special considerations
-Renal colic and AAD sound a lot alike
-STEMI and AAD can occur at the same time -> Dissect right into the RCA (uncommon)
-What if I’m not sure if its PE vs. AAD?
-Institution dependent, call your radiologist!
-Most hospitals: CTA with PE protocol, as it can also assess for dissection
-Oops, I gave the chest pain patient ASA, and they have AAD
-Nothing proven (yet) that 325mg ASA has poor outcomes
-Heparin and tPA though… bad
A 60-year-old man presents with retrosternal chest pain…The patient reports that he’s had chest pain for 2 days that has been constant and never goes away.
He has no dyspnea, diaphoresis, or radiation of the pain. Additionally, there is no increase in the pain with exertion.
You obtain an ECG and note ST-segment elevation in the inferior and lateral leads.
Given the patient’s history of present illness, you are not convinced that he has STEMI and wonder what the best next step is…
Based on this patient’s presentation, you were not convinced that he had ACS, despite ST elevation noted on the ECG.
You noted that there was no reciprocal ST depression found anywhere on the ECG tracing. You also noted that all ST elevation was in a concave, upward pattern and was rather diffuse.
You asked the patient to lie supine, and he stated that the pain got worse.
Based on the fact that the patient had constant chest pain not associated with diaphoresis, vomiting, or radiation, along with your evaluation of the ECG, you decided to not activate the cardiac catheterization lab.
Instead, you discussed the case with the interventional cardiologist, and said you were more concerned that the patient had pericarditis rather than STEMI. The cardiologist agreed with your assessment.
You recommended a formal echocardiogram be performed in the ED, and she agreed. You obtained the study, which showed no wall motion abnormality, but did show a moderate pericardial effusion, thus confirming your suspicion of pericarditis.
He has no dyspnea, diaphoresis, or radiation of the pain. Additionally, there is no increase in the pain with exertion.
You obtain an ECG and note ST-segment elevation in the inferior and lateral leads.
Given the patient’s history of present illness, you are not convinced that he has STEMI and wonder what the best next step is…
Based on this patient’s presentation, you were not convinced that he had ACS, despite ST elevation noted on the ECG.
You noted that there was no reciprocal ST depression found anywhere on the ECG tracing. You also noted that all ST elevation was in a concave, upward pattern and was rather diffuse.
You asked the patient to lie supine, and he stated that the pain got worse.
Based on the fact that the patient had constant chest pain not associated with diaphoresis, vomiting, or radiation, along with your evaluation of the ECG, you decided to not activate the cardiac catheterization lab.
Instead, you discussed the case with the interventional cardiologist, and said you were more concerned that the patient had pericarditis rather than STEMI. The cardiologist agreed with your assessment.
You recommended a formal echocardiogram be performed in the ED, and she agreed. You obtained the study, which showed no wall motion abnormality, but did show a moderate pericardial effusion, thus confirming your suspicion of pericarditis.
pericarditis etiology
-Infectious:
-Viral, bacterial, TB, fungal
-Non-infectious:
-Post MI: Dressler’s syndrome
-Connective tissue disease
-Autoimmune disease
-Neoplasm
-Metabolic: Uremia
-Trauma: Penetrating, radiation
-Medication induced
pericarditis manifestations
-Symptoms
-!substernal chest pain
-pleuritic chest pain that increases with deep inspiration or yawning, swalloing, rotating trunk
-sharp and pleuritic
-Relief with sitting up and leaning forward
-Dysphagia
-Fever
-Malaise
-lasts 2-4 weeks
-Physical exam
-!Friction rub (best heard when sitting up leaning forward) -> rare
-Tachycardia
-Pulsus paradoxus (BP down when inspiring)
-imaging findings:
-!ECG: New widespread ST segment elevations or PR depressions
-!US/echo: New or worsening pericardial effusion!
-CXR- usually normal
DX of pericarditis criteria
-Diagnosis of percarditis requires 2/4:
-Chest pain consistent with pericarditis- Classically sharp and pleuritic
-Friction rub (rare)
-Typical ECG changes - Diffuse STE (not in V1 or aVR, that makes pericarditis unlikely)
-Pericardial effusion on ultrasound
complications of pericarditis
-dysrhythmias
-Tamponade
-Residual pericardial constriction
-Heart failure
pericarditis tx
-Underlying cause if possible
-Anti-inflammatories: NSAIDs , ASA or steroids (tapered over 2-4 weeks)
-Dispo
-Uncomplicated without effusion: Outpatient with close follow up and clear instructions regarding anti-inflammatory tapers and avoiding exercise
-Effusion, perimyocarditis, intractable pain, constrictive pericarditis should be monitored inpatient with continuous telemetry and serial echocardiograms
-it is critical to consider acute myocardial ischemia before concluding a final dx of pericarditis
Which of the following statements about pericarditis is FALSE?
can be a complication of MI
It may be associated with acute renal failure
There is inflammation of the sac covering the heart
It causes systolic dysfunction
Symptoms may present after an upper respiratory tract infection
can be a complication of MI
It may be associated with acute renal failure
There is inflammation of the sac covering the heart
It causes systolic dysfunction
Symptoms may present after an upper respiratory tract infection
-It causes systolic dysfunction!!!
-fibrinous -> restrictive pericarditis -> cant relax -> diastolic dysfunction
Which ECG changes are NOT associated with acute pericarditis?
Normalization of ST segments after the first week
Q waves
PR elevation in lead aVR
ST elevation in most leads
PR depression in most leads
Normalization of ST segments after the first week
A 30yoM without PMH presents with progressively worsening chest pain over 3 days…
Recent URI
Mild fluid overload
A 22yoF with suspected myocarditis one month ago presents to the ED with a cough…
A 40yoM with an out-of-hospital cardiac arrest…
waves
ST elevation in most leads
PR depression in most leads
myocarditis
waves
Recent URI
Mild fluid overload
Patients with acute myopericardial syndromes may exhibit varying levels of clinical stability. Vital signs may initially be normal or abnormal and non-specific (ie, unexplained tachycardia or tachypnea).
clinical manifestations of myocarditis
-Often associated with pericarditis, this is inflammation of the myocytes of the heart.
-Myocarditis + cardiac dysfunction = inflammatory cardiomyopathy
-causes:
-Infectious (usually viral)- Consider protozoan agent (Trypanosoma cruzii, aka CHAGAS disease) which is the most common cause worldwide
-Drugs (chemotherapy, antipsychotics like clozapine)
-Toxins (alcohol, carbon monoxide, cocaine)
-Immunologic (pancarditis from acute rheumatic fever)
-Idiopathic
dx of myocarditis
-“Flu like” illness (myalgias, fatigue, joint pains, recent viral illness)
-“ACS-like” chest pain 1-4 weeks after respiratory or GI illness
-± New onset or worsening heart failure symptoms (SOB, palpitations, DOE. Edema, new murmur, hepatomegaly)
-Vitals: Fever, Out of proportion tachycardia
-Dysrhythmias (sinus tach, PACs, ventricular extra-systoles are common)
-Sudden death- Cause of sudden death in up to 20% of young adults
ldaksj
-No ECG findings are specific
-sinus tachycardia -MC
-Cardiac damage can cause atrial and ventricular arrythmias (afib and vtach MC)
-signs of ischemia -> diffuse t waves inversions, saddle shaped ST elevation
-non-specific ST changes
-Labs:
-Troponin elevation (if within time frame)
-Elevated markers of inflammation -> CRP, ESR
-imaging:
-Cardiac MRI visualizing marker of myocardial inflammation
-def dx is histological:
-Endomyocardial biopsy is the gold (and impractical) standard
lkjasdf
diffuse t wave inversion in myocarditis
tx and dispo of myocarditis
Diffuse ST segment elevation in saddle-back shape without reciprocal changes in myocarditis
pericardial tamponade: causes, sx, imaging
-Dispo
-admit all pts to a monitored bed for serial echocardiograms and troponins
-ICU if hemodynamic instability
-Treatment
-Symptomatic treatment
-cardiogenic shock with IV fluids, respiratory support, vasopressors, inotropes
-Restriction of exercise at least 6 months
-Consider AICD, ECMO, LVAD if cardiac support required
-Myocarditis is scary! It can lead to sudden cardiac death in otherwise young healthy persons. There isn’t much to do to prevent this
tips
-Causes:
-Acutely from: trauma or aortic injury
-Slow from: Pericarditis, infection, neoplasm
-Clinical signs:
-Hypotension
-JVD
-Muffled heart sounds
-Pulsus paradoxus
-CXR: enlarged water bottle heart in chronic effusion. (Acute will have normal appearing silhouette) -> doesnt rule it out
->300ml until you see it on CXR
tricks
-ECG low voltage
-electrical alternans present is less than a third of tamponade pts -> alternating QRS (swinging)
POCUS signs for pericardial tamponade
swinging heart
tamponade tx
-!Pericardial effusion
-!RV diastolic collapse is specific for tamponade -> due to high pressure
-Plethoric inferior vena cava and/or severely depressed left ventricular (LV) contractility
tips
-ABCs
-Caution in mechanical ventilation, which ↑ intrathoracic pressure and thus ↓ preload
-2 large bore Ivs, Monitoring, ECG, O2
-Give fluids! They are preload dependent!
-!!!!Unstable: Emergent pericardiocentesis
-Stable: Echo/CT/fluoroscopy guided pericardiocentesis or pericardial window
-There are no absolute contraindications to this pericardiocentesis, as pericardial tamponade can deteriorate into cardiac arrest.
