chest pain Flashcards

Question

STEMI criteria

Answer 1

-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

Answer 2

STEMI ACUTE ANTERIOR INFARCT -anterior septal MI -V4- tombstones

Answer 3

STEMI LATERAL WALL -left circumflex artery -reciprocal changes in 2,3,aVF -> confirms the STEMI

Answer 4

-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

Answer 5

-preload dependent = tx with IV fluids -nitrates are contraindicated -some do a right sided ECG -> flip it

Answer 6

Anterior ischemia  possible posterior STEMI. You noticed ST depression in leads V2 and 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 V7 and 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.

Answer 7

stemi posterior wall -aka inferobasal stemi -infer you are seeing the a posterior MI when you see reciprocals -V1 and V2 depression

Answer 8

-Rare (3% of MI) ->2 mm STD in V1-V4 -Tall R waves (R:S >1) -look at 7,8,9 -!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

Answer 9

-these are complete occlusions -> BAD -DeWinter T-waves -Isolated ST elevation in aVR -upsloping ST depressions in precordial leads -LAD occlusion -completely occlusive LAD -call cardiac cath -LBBB showing a STEMI equivalent via Modified Sgarbossa criteria -Wellens

Answer 10

STEMI in AVR (De winter)

Answer 11

wellens pattern -strongly assoc with LAD occlusions !!!! -deep wide symmetrical t wave inversion in the precordial leads (V1-6)

Answer 12

-left bundle branch block -how do you know this isnt a STEMI -> you dont -> look at criteria

Answer 13

-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

Answer 14

-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

Answer 15

-ischemia- + QRS and positive ST segement elevation -> going the same way -A. more than 25% -> ischemic

Answer 16

-criteria 1 -> no -criteria 2 -> V2 and V3 -> concordanant ST depression YES -this is ventricular paced with ischemia

Answer 17

-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

Answer 18

-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

Answer 19

-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!*

Answer 20

DONT USE -morphine masks pain -O2 only if needed -Nitrates arent given in RV or inferior MI -aspirin is good

Answer 21

-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

Answer 22

-!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

Answer 23

-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!!!!

Answer 24

-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

Answer 25

-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

Answer 26

-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

Answer 27

-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

Answer 28

risk stratification: HEART score

Answer 29

-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

Answer 30

-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

Answer 31

-“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!

Answer 32

Peri-infarction pericarditis Pericardial effusion due to myocardial rupture -Dressler syndrome (post cardiac injury syndrome)!!!!!!!!!!! Pericardial tamponade Fibrinous pericarditis

Answer 33

Assessment 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

Answer 34

type A dissection extending into the aortic bifurcation

Answer 35

-A rare, deadly, and confounding diagnosis -~40% are initially missed -Mortality is 40% in acute phase, 70% in two weeks

Answer 36

-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

Answer 37

-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 -High blood pressure -High heart rate

Answer 38

-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

Answer 39

-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

Answer 40

-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

Answer 41

-Definitive management depends on type of dissection -Stanford A - Emergency SURGERY (CT surgery) -Stanford B - Endovascular stenting and Medical management -Anticoagulation and fibrinolysis = bad!

Answer 42

-!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

Answer 43

-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

Answer 44

-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

Answer 45

-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

Answer 46

-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

Answer 47

-dysrhythmias -Tamponade -Residual pericardial constriction -Heart failure

Answer 48

-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

Answer 49

-It causes systolic dysfunction!!! -fibrinous -> restrictive pericarditis -> cant relax -> diastolic dysfunction

Answer 50

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).

Answer 51

-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 MCC worldwide -Drugs (chemotherapy, antipsychotics like clozapine) -Toxins (alcohol, carbon monoxide, cocaine) -Immunologic (pancarditis from acute rheumatic fever) -Idiopathic

Answer 52

-“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

Answer 53

-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

Answer 54

diffuse t wave inversion in myocarditis

Answer 55

Diffuse ST segment elevation in saddle-back shape without reciprocal changes in myocarditis

Answer 56

-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

Answer 57

-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

Answer 58

-ECG low voltage -electrical alternans present is less than a third of tamponade pts -> alternating QRS (swinging)

Answer 59

swinging heart

Answer 60

-!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

Answer 61

-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.