Chest Pain 2 Flashcards

Question

Approach to PE

Answer 1

-Blood work -Routine labs for CT imaging- CBC, BMP, Creatinine -D-dimer -Sensitivity 97% -Specificity 39% -Age adjusted dimer >50 yo: here -Troponin- Prognostic marker for RV dysfunction and death -BNP- Prognostic marker for RV dysfunction -ECG -CXR -CT pulmonary angiography -V/Q scan -echo -doppler US -

Answer 2

-ECG is mostly non-specific -Sinus tachy (30-40%) and non-specific ST and T wave changes is most common -Look for signs of right heart strain -RBBB (20%) -S1Q3T3 (10%) -Deep TWI V1-V4 (30%) -Rightward axis (large S in lead I) -Assess differentials for these changes

Answer 3

-Assess differentials (PNA, effusion, PTX, CHF) -!!!CXR in PE are usually normal -Non-specific atelectasis, pleural effusion, elevated hemidiaphragm -Rare CXR findings in PE -Hampton’s hump or Wedge infarct -Westermark’s sign

Answer 4

-CT pulmonary angiography -Imaging test of choice! -Detects filling defects -Evaluate for PE and others -V/Q scan -PE = Ventilation without perfusion -Similar sensitivity and specificity to CT chest -Cannot determine alternative etiology -Requires good technique -Pregnant pts can do a perfusion only scan if concerns for adverse reactions to contrast agents

Answer 5

High probability VQ scan for PE

Answer 6

-ECHO -May show right heart strain -“D” sign - right heart strain -> shifts the LV making it a D shape -Doppler U/S -If suspicious of DVT -Assess for differentials (Cellulitis, cyst)

Answer 7

Systemic anticoagulation!!!!!! Morphine, aspirin, oxygen Pulmonary embolectomy (only massive) Direct thrombolytic therapy (only massive) -if pt is stable -> anticoagulation -if pt is unstable -> thrombolysis

Answer 8

-Classification of PE can be anatomic or hemodynamic. In the acute care setting, hemodynamic classification is the most useful: -Massive (high risk): Persistent Hypotension, bradycardia, cardiac arrest, and right ventricular outflow obstruction (ultrasound finding). -Submassive PE with hemodynamic compromise is often treated like massive PE. -30 day mortality is ~50% for massive PE -Submassive without hemodynamic compromise (intermediate risk): Evidence of right ventricular obstruction or myocardial damage without hemodynamic compromise. -Low risk: No end-organ damage or right ventricular strain or hemodynamic instability.

Answer 9

-ABCS first! -Low risk without right heart strain + hemodynamically stable: -Apply HESTIA score to see if low risk for outpatient management -!!!Anticoagulation for at least 3 months with either -!DOAC is preferred treatment (table 1 here) or -!!Bridge to WARFARIN with UFH/LMWH -Hemodynamically Unstable: -Thrombolysis and/or embolectomy (surgery) -IVC-filter rarely indicated, lacking safety/effective data -dont memorize chart

Answer 10

-ACS- ECG, Troponin, CXR, HEART score -PE- Wells, Geneva, PERC, Dimer, ± CT -PNA and PTX- Vitals, Exam, CXR -Booerhaeves- Good history, exam, and CXR -Tamponade- Good history, exam, U/S -Aortic dissection- Good history, AAD score, Dimer

Answer 11

-ABCs -No contraindications for RSI meds in pregnancy -If > 20 weeks gestation: left lateral tilt position or manually displace the uterus to the left -All chest pain related disorders can happen in pregnant patients! -PE -Pregnancy is a risk factor for PE -No validated pre-test clinical probability tools (though YEARS criteria is promising) -D-dimers progressively increase over the course of pregnancy, no consensus on cutoffs for this group -V/Q scan or CT pulmonary angiography for diagnosis -Pregnancy CAN get thrombolytics if necessary -Admission for LMWH for non-massive PE -ACS -Same algorithm except for using thrombolytics (this is since coronary artery dissections look exactly like a STEMI, and thrombolytics would worsen the dissection) -Aortic Dissection

Answer 12

-Sudden and !brief loss of consciousness and muscle tone! due to !decrease in cerebral blood flow! -Followed by !spontaneous recovery to normal mentation! -Up to 50% of people in the USA will have it at least once in their lifetime -Do NOT confuse with a seizure

Answer 13

-Most important parts are the history, exam, ECG and glucose level -History: -Ask about: situation, chest pain, shortness of breath, medications, recent illness, prodrome, family history of sudden death -Exam: -Heart rate, rhythm, murmurs, carotid bruits, neurologic exam -Signs of trauma from the syncopal episode -1. ECG in every syncope patient -2. BLOOD GLUCOSE LEVEL in every syncope patient -3. Cardiac monitor while being evaluated in ED

Answer 14

-ARVD- Arrhythmogenic right ventricular dysplasia -Brugada- Brugada syndrome -LVH - Left ventricular hypertrophy (Aortic stenosis, HOCM) -PE- Pulm embolism -QTc- Too long or too short -WPW- Wolf Parkison White

Answer 15

-Genetic cardiomyopathy -#2 cause of sudden cardiac death -RV myocardial cells are slowly replaced by fat/fibrous tissue -> thinning ventricular wall and dilation -Occurs usually in 3rd-4th decades of life -Be highly suspicious in patients who present with symptoms during physical activity: palpitations, syncope, cardiac arrest -ECG findings: (dont need to know) -!T wave inversion in right precordial leads -V1-3, in absence of RBBB (85% of patients) -!Epsilon wave (most specific finding, seen in 50% of patients) -Localised QRS widening in V1-3 (> 110ms) -Prolonged S wave upstroke of 55ms in V1-3 -Ventricular ectopy of LBBB morphology, with frequent PVCs > 1000 per 24 hours -Paroxysmal episodes of ventricular tachycardia (VT) with LBBB morphology (RVOT tachycardia)

Answer 16

-Cause of syncope -Common to young, South Asian men (but also found in general population) -Responsible for 20% of sudden cardiac deaths -Rare genetic disorder affecting mostly RV -Restricts flow of Na+ ions into the heart -Does NOT affect the structure of the heart (intact) -Episodes of mono/polymorphic VT -Leads to V. Fib and cardiac arrest

Answer 17

-Left ventricle enlarges due to pressure overload -Aortic stenosis, hypertension -Though not exactly the same, think HOCM -Have EXERTIONAL symptoms -ECG- large overlapping QRS -Markedly increased LV voltages: huge precordial R and S waves that overlap with the adjacent leads (SV2 + RV6 >> 35 mm). -R-wave peak time > 50 ms in V5-6 with associated QRS broadening. -LV strain pattern with ST depression and T-wave inversions in I, aVL and V5-6. -ST elevation in V1-3. -Prominent U waves in V1-3. -Left axis deviation

Answer 18

-Structural change with left ventricular hypertrophy that occurs without inciting stimulus such as HTN or aortic stenosis -!!!Asymmetric thickening of the anterior interventricular septum -MCC of sudden cardiac death in <40yo -Associated with: Exertional syncope/pre-syncope, pulmonary congestion (exertional dyspnea, fatigue, orthopnea, PND), chest pain, palpitations -Classic HCM ECG: -Signs of LVH (increased precordial voltages) -Deep, narrow, “dagger-like” Q waves in lateral ± inferior leads

Answer 19

Pulmonary embolus

Answer 20

Prolonged QT -the QT is more than half the RR

Answer 21

-Channelopathy -Short QT interval (<340ms) -!!No change in QT with heart rate -Peaked precordial T waves -Treatment with AICD

Answer 22

-Congenital accessory pathway (!bundle of kent!) connects atria to ventricles, bypassing AV node -Causes tachyarrhythmias and sudden death -ECG findings in WPW: -Short PR interval (<120ms) -Wide QRS (>100ms) -Slurred upstroke of the QRS (delta wave!)

Answer 23

-!ECG, Glucose, [Monitor] – only “routine” things to check -Labs if indicated -Glucose, pregnancy, CBC/CMP, T&S, Cardiac enzymes -!!CT head is NOT routinely indicated! … unless suspicion of neurologic cause -Of the rules, the !Canadian syncope risk score! is the best (but not better than your own H&P) -Young and otherwise healthy people with normal exams and vagal-type story, normal Ecgs rarely need any further evaluation (CT heads, CXR, labs etc.)

Answer 24

CLINICAL SYNDROME with -1. END ORGAN DAMAGE: -HEART (angina, CHF, dissection) Brain (encephalopathy, hemorrhage) Eyes (hemorrhages, exudates) Kidneys (failure, preeclampsia) + -2. SEVERELY ELEVATED BP: -No specific BP level definition (but often >180/120) -That requires immediate reduction of BP

Answer 25

-Heart -brain -kidney -other

Answer 26

-MORE LIKELY IN… -Persons >60 years old, Black, Males, Uninsured or underinsured, Persons who live in lower socioeconomic areas -THE MOST COMMON CAUSE -!ABRUPT! INCREASED BP IN PATIENTS WITH UNDERLYING CHRONIC HTN -Medication noncompliance -Withdrawal syndromes e.g. clonidine cessation causing ↑ HR/BP -Stimulant intoxication, cocaine, methamphetamine, and phencyclidine -Not-so common causes -Pheochromocytoma (intermittent episodes of sweating, HA, anxiety, tachycardia and ↑ BP) -Adverse drug interactions

Answer 27

-Diagnostic studies should focus on areas that may reveal end organ damage -Renal function -Glucose, CTH if neuro changes -Pregnancy test -ECG if chest pain, palpitations, shortness o breath -CXR for pulmonary edema -POCUS for edema, dissection, bladder outlet -POCUS the eye for papilledema (IIH)

Answer 28

-1st hour- reduce MAP by 25% -Next 2-6 hrs - Reduce 5-15% more -48 hrs - “Normal” -ex: -BP = 238/125 -[238+(2x125)]/3 = 162.7 -25% reduction in MAP 122 -still high goal 180/93 -DONT GO UNDER THAT

Answer 29

-BETA BLOCKERS -FIRST LINE -Labetalol: -Beta-blocker + alpha blocker (B>>A) -Onset 5-10 minutes. -Half life 5.5 hours -Contraindicated: Asthma, bradycardia, heart blocks, acute CHF, COPD -Esmolol has more impact on HR than BP and often used for aortic dissection -CCB -Nicardipine: -Calcium channel blocker -Onset 10-15 minutes -Half life is 1-4 hours -Easily titratable in IV form -Great for intracranial emergencies -Contraindication: Aortic stenosis -Diltiazem (more chronotropic) -DIRECT VASODILATORS -Nitroglycerin -Vasodilator (greatly preduces preload) -Onset 2-5 minutes -Duration 3-5 minutes -Contraindicated: Phosphodiesterase 5 inhibitor use

Answer 30

-Ischemic stroke -(+)getting tPA 🡪 GOAL: <185/110 before tPA and maintain <180/105 for 24 hrs -(-)getting tPA 🡪 GOAL: <220/120 SBP -Hemorrhagic stroke -SBP <140 in first hour (maintain between 130-150mmHg) -Aortic dissection -HR 60-80bpm THEN SBP <120mmHg in first hour (Esmolol most common) -Pre-eclampsia (pregnant) -<140 in 1st hour -dont memorize the number- know the concept

Answer 31

Based on the patient‘s history of CHF and physical exam, you believed that he was having acute “flash” pulmonary edema. POCUS showed bilateral B-lines CXR showed cardiomegaly with pulmonary congestion. Immediate BiPAP and high-dose nitroglycerin infusion, with relief of symptoms. The patient was given furosemide IV and was admitted for further management of his flash pulmonary edema.

Answer 32

IV lorazepam for his seizure STAT CT head = normal Bedside ocular ultrasound showed evidence of papilledema, raising concern for cerebral edema. MRI showed posterior cerebral edema, confirming the diagnosis He was treated for PRES with a nicardipine infusion.

Answer 33

NEW TERMS Severe hypertension SBP >= 180 mm Hg DBP >= 110 mm Hg MAP >=135 mm Hg Hypertensive emergency Above PLUS rapidly evolving end organ damage You recheck BP with automatic cuff after leaving her alone for 5-10 minutes… it is unchanged You obtained extensive PMH, social, and family history, and found no increased risk factors for hypertensive emergency. ROS and PE, including visual acuity, was unremarkable. Based on your clinical evaluation, you had very low concern for end-organ damage. Discussed strict return precautions with the patient and advised her to follow up with her primary care doctor in the next few days for a repeat evaluation. Reassurance was given

Answer 34

->160/100 mmHg falls into this category -Severe BP elevation in otherwise stable patients without acute or impending change in target organ damage or dysfunction -There is no indication for referral to the emergency department, immediate reduction in BP in the emergency department, or hospitalization for such patients

Answer 35

-Documentation for a patient thought to have elevated BP without evidence of an end-organ damage hypertensive emergency should include a specific mention of the physical exam maneuvers that evaluated for this evidence, such as documentation supporting no evidence of: -chest pain, shortness of breath or pulmonary rales, neurologic changes, papilledema or fundoscopic abnormalities, changes in urination, or lower extremity edema.

Answer 36

Working diagnosis: CHF w/ pulmonary edema Treatment: IV diuretics, BiPAP ordered, go to CXR Labs returned: leukocytes 6.4, hemoglobin 8, platelet 165, sodium 140, potassium 5.0, chloride 101, creatinine 120, urea 11, glucose 170. Venous blood gas showed pH 7.31, pCO2 55, HCO3- 28 and lactate 2.7. CXR returned:

Answer 37

-RV collapse

Answer 38

Initial MDM from provider: Diagnosis management comments: 61 y/o female patient with history of scleroderma (multiple GI complications), ILD, hypothyroidism, GERD, depression, previous pericardial effusion and bowel resection presenting for back pain and leg pain from sacral and heel decubs. Concern for PNA, a-fib. -Labs -EKG -CXR -consider CT chest for PE Dispo: likely admit -Patient had a cardiac arrest Emergent pericardiocentesis with 250cc bloody fluid drainage ACLS without rosc Patient died