quiz 1 - chest pain 2 Flashcards
A 35-year-old man who uses intravenous drugs presents to the ED with fever, chest pain, dyspnea x 2 weeks and low back pain x 2 days.
Vitals: HR 114bpm, RR 20, Temp 100.3F, BP 110/79 mmHg, Spo2 97%
Lung exam: Crackles diffusely, bilaterally
Back exam: Paraspinal tenderness in lumbar region
Neuro exam: Normal
Vitals: HR 114bpm, RR 20, Temp 100.3F, BP 110/79 mmHg, Spo2 97%
Lung exam: Crackles diffusely, bilaterally
Back exam: Paraspinal tenderness in lumbar region
Neuro exam: Normal
large pleural effusions
-nodules circled
Infective carditis: causes and RF
-Rare
-Mitral and aortic -MC unless a IV drug user
-Endocardium inflammation from infection
-Staphylococcus aureus (31%)
-Viridians streptococci (17%)
-HAECK group
-Vegetations form:
-Endocardial surface of the heart
-Heart valves
-Endocardial devices
-Risk factors:
-Prosthetic cardiac material
-Intravascular device
-Congenital heart defects
-History of IE
-Male sex
->65 years old
-IV drug use
-Chronic hemodialysis
Infective carditis: S&S
-!Fever (90%)- can be only sx
-Flu-like illness (chills, headaches, night sweats)
-Cardiac murmur (85%)
-Heart failure from valve regurgitation
-Left sided: Systemic emboli (ischemic stroke, kidney infarcts)
-Right sided: Septic pulmonary emboli
-Signs of local infection at the site of pacemaker/catheter
-Immunologic phenomena: Glomerulonephritis, Osler’s nodes, Roth spots
-Vascular phenomena: Arterial emboli, Septic pulmonary infarcts, mycotic aneurysm, ICH, Janeway lesions
Infective carditis: dx
-Dx:
-Echocardiogram
-TTE 70% sensitivity for native valve endocarditis
-TTE 50% sensitivity for prosthetic valve
-TEE 92-96% sensitivity for either
-Valvular regurgitation -> Especially if new, or, in someone young who should not have it
-Thickened valve
-Vegetation on valve
-Prosthetic valve partial dehiscence
-Blood cultures *
-Histopathologic evidence of endocarditis
-Modified Duke Criteria- dont memorize
Infection endocarditis complications
-Normal exam ≠ no pathology
-Cardiac: Valvular insufficiency, acute heart failure, shock, pulmonary edema.
-CNS: Embolic stroke, hemorrhagic stroke, meningitis, brain abscess, intracerebral hemorrhage.
-Pulmonary: Septic pulmonary emboli.
-Vascular: Acute arterial occlusion.
-Renal: Renal failure and glomerulonephritis.
-Metastatic infections: Septic arthritis, discitis, osteomyelitis, psoas abscess
endocarditis management
-DONT MEMORIZE THIS JUST GENERAL
-Tx in ED starts with antibiotics, for 6 weeks
-Native valve endocarditis (no IVDU)
-!Vancomycin (20-35 mg/kg/dose loading, max 3g) (alternative daptomycin)
-PLUS gram negative coverage (Cefazolin 2g IV q8 hours, or ceftriaxone, ampicillin-sulbatam, ciprofloxacin)
-Native valve endocarditis (IVDU or sepsis)
-Vancomycin
-PLUS gram negative coverage with anti-pseudomonal activity (cefepime 2 g IV q8h, ceftazidime, meropenem, piperacillin-tazobactam)
-Prosthetic valve
-!Vancomycin PLUS Gentamycin PLUS either cefepime/ciprofloxacin!
-!Surgical intervention
-Who do you call? Cardiothoracic surgery!
-Heart failure with valve insufficiency
-New murmur consistent with severe aortic/mitral valve insufficiency
-Echocardiographic evidence of valvular dysfunction
55-year-old man with a history of alcohol use disorder presents with severe chest pain that started immediately after vomiting.
145/90mmHg, HR 102, RR 22, SPO2 96%, Temp 98.6F
Exam reveals crunching sounds over the heart
Crepitations over the neck
145/90mmHg, HR 102, RR 22, SPO2 96%, Temp 98.6F
Exam reveals crunching sounds over the heart
Crepitations over the neck
ESOPHAGEAL RUPTURE
A 45-year-old presents 2 days after an upper endoscopy with retrosternal chest pain, midback pain, and odynophagia.
He is hypotensive and tachycardic
He is hypotensive and tachycardic
-PNEUMOPERITONEUM
Esophageal rupture
-if spontaneous -> aka booerhaaves
-Transmural defect that occurs in the esophagus, exposing the mediastinum to GI content.
-Causes:
-!Iatrogenic (endoscopy, surgery) * MC
-Spontaneous (called Boerhaave syndrome)- heavy wts, vomiting, coughing
-!Foreign body ingestion (trauma)
-!Forceful vomiting
-Esophageal or mediastinal malignancy
-Intrinsic disease of esophagus: Crohns, esophagitis (pill, infectious, eosinophilic)
-Mortality rate: 10-50%
Esophageal rupture sx
-Acute onset
-MACKLER TRIAD with Boerhaave syndrome:
-!Vomiting followed by
-!Severe retrosternal chest pain and
-!!!Subcutaneous emphysema
-Varying symptoms depending on location:
-Retrosternal chest pain- thoracic
-Neck pain
-Back pain- thoracic
-Dysphagia or odynophagia- cervical
-SOB
-Abdominal pain- lower
-Fever
-should be considered in any pt who has neck pain, back pain, odynophagia, dysphagia, dyspnea, or fever after endoscopy or esophageal instrumentation
Esophageal rupture exam findings
-Tachycardic, tachypneic or dyspneic
-Diaphoretic
-!Crepitus in neck or chest (<60%)
-Hamman’s crunch - Audible crepitus on auscultation of the precordium with heart beat (rare)
-Reduced breath sounds on side of perforation
-Abdominal tenderness in lower esophagus perforation
-Severe and or late presentation: Fever, tachycardia, hypotension, ill-appearing with signs of septic shock
Esophageal rupture complications
-Acute mediastinitis
-Acute inflammation of the mediastinal tissues due to mediastinal spread of the esophageal and oropharyngeal flora
-Presents with severe retrosternal chest pain, fever, tachypnea, tachycardia, or septic shock
-Sepsis if delayed presentation.
-Pleuritis
-Pericarditis
-Empyema: a collection of pus in the pleural cavity
Esophageal rupture imaging
-Cervical X-RAY
-If suspected cervical esophageal rupture, looking for subcutaneous emphysema
-Chest X-RAY
-Pneumomediastinum (shown)
-Pneumopericardium
-Pneumothorax
-Pleural effusion
-Widened mediastinum
-Subdiaphragmatic air
-CT esophagram with water soluble contrast is the modality of choice (gastrografin)
-Extravasated contrast/air
-Free air/fluid
-Esophageal wall thickening
-Pneumomediastinum
-Pneumopericardium
-Pneumothorax
-Widened mediastinum
CT esophagram with water soluble contrast
-esophagus is in front of the esophagus -> dye is spilling out
Esophageal rupture management
-Initial approach:
-ABCDE survey:
-Airway: Ensure the patency of the airway
-Breathing: Ensure proper ventilation is occurring.
-Circulation: Measure blood pressure and pulse, and administer IV fluids
-Disability: Perform basic neurologic examination.
-Exposure: Search for injuries and perform environmental control.
-!Nothing by mouth (NPO)
-!Broad-spectrum IV antibiotics
-IV analgesic
-IV proton pump inhibitor
-Parenteral nutrition
-!Obtain surgical (cardiothoracic) consult
-Further intervention determined by:
-Size and location of perforation
-Comorbidities
Esophageal rupture key concepts
-can range from small to large rupture, leading to a variety of clinical presentations.
-MC etiology of an esophageal perforation is iatrogenic as a result of endoscopic interventions.
-The Mackler triad for spontaneous rupture includes vomiting followed by chest pain and the presence of subcutaneous emphysema. This triad is only present in less than 50% of patients.
-The morbidity and mortality rates of esophageal rupture are high and are directly related to delays in diagnosis and management. Perforations diagnosed within the first 24 hours have the highest rate of survival.
-Broad-spectrum antibiotics, consultation with thoracic surgery, and ICU admission are critical components in the management of patients with spontaneous rupture (Boerhaave syndrome).
A 45-year-old with history of a recent orthopedic surgery presents with abrupt-onset pleuritic chest pain and shortness of breath. He is hypoxic and hypotensive.
A 36-year-old female presents with 2 days of shortness of breath. She is hemodynamically stable, has normal right ventricular function on ultrasound, and a negative troponin. CT reveals subsegmental pulmonary embolism
-1. massive PE
-2. low risk PE
Approach to critical pt due to PE
-AIRWAY
-Avoid intubation !when possible!
-Obstructive shock and hemodynamic collapse are primary reasons for deterioration (not respiratory failure)
-Intubation can precipitate large drop in preload
-Consider early use of pressors before intubating (to increase preload)
-BREATHING
-Avoid hypoxemia and hypercapnia
-Consider high flow nasal cannula ± nebulized nitroglycerin
-CIRCULATION
-Avoid hypotension – use pressors early!
-Avoid excessive fluids (can worsen RV distension and cardiac output)
-Consider ECMO
-Systemic thrombolysis
-Cardiac arrest
-Massive PE and unstable
-Catheter directed thrombolysis and thrombectomy
-Open surgical thrombectomy
Pulmonary embolism
-OBSTRUCTION in the pulmonary arterial tree
-!Thrombus is MC (leg DVT -> lungs)
-Air
-Fat from long bone fractures
-Tumor material from malignancies
-Range from asymptomatic to acute obstructive shock and !sudden cardiac arrest !
-Respiratory problems: V/Q mismatch
(ventilation but no perfusion)
-Cardiac problems: ↑ PVR causing RV strain ± failure
PE stats
-50% no risk factors
-3rd MC cause of CV death
-1/500-1000 ED patients
-30% no perception of CP
-60% of pts w/ DVT have PE
-90% of pts with PE develop from DVT above the level of the popliteal
PE S&S
-Symptoms are typically rapid in onset and progressive -> But can range from chronic to subacute to acute
-Asymptomatic
-Chest pain (50%)
-SOB (80%)
-Leg swelling
-Flank or upper abdominal pain (pleuritis from pulmonary infarct)
-Syncope
-Cardiac arrest
-Patients may exhibit air hunger and behavioral oddities that can easily be mistaken for anxiety and panic.
PE: getting a hx
-Prior VTE / anticoagulation
-Family history of hypercoagulable state
-Recent surgery
-Trauma to LE or pelvis in last 3 months
-Prolonged bed rest or immobilization (travel, hospital admission)
-History of Malignancy
-Smoking cigarettes
-Oral contraceptives (estrogen)
-Testosterone therapies
-Pregnancy
-Venous foreign body (central line, PPM)
-virchows triad:
-Stasis / Immobilization
-Hypercoagulability
-Endothelial damage
-+AGE
Pulmonary embolism: PE
VITALS:
↑ HR
↑ RR
↓ BP
↑ Low grade temp
↓ O2 sat (<94% in 74% of pts)
-HEART:
-JVD
S3/S4
-LUNGS:
-Normal
-May have rales, wheezing, dullness to percussion, fremitus, decreased breath sounds
-PERIPHERAL:
-Leg edema
-Calf tenderness
-Erythema or warmth
PE: clinician decision aids
-Risk stratification with:
-Well’s score (classic) or
-Revised Geneva score (more objective)
-YEARS score (pregnancy)
-If low risk, rule out PE with the PERC score:
PERC score
Approach to PE
PE: investigation
-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
-
PE: ECG
-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
PE: CXR
-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
PE: CT pulmonary angiography and V/Q scan
-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
High probability VQ scan for PE
PE: echo and doppler US
-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)
A 49-year-old man presents with sudden onset chest pain and shortness of breath for 2 hours. A CT chest reveals pulmonary emboli. The next best step in treatment is…
Systemic anticoagulation!!!!!!
Morphine, aspirin, oxygen
Pulmonary embolectomy (only massive)
Direct thrombolytic therapy (only massive)
-if pt is stable -> anticoagulation
-if pt is unstable -> thrombolysis
PE classification- dont need to know
-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.
Tx if PE
-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
Approach to chest pain summary flow chart
ladskjfsadf
Remember our evidence based clinical decision tools and sensitive initial tests
-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
Chest pain and pregnancy
-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
Syncope
-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
Syncope work up
-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
Syncope: ECG
-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
ARVD
-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)
Brugada syndrome
-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
Brugada
LVH
-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»_space; 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
Hypertrophic cardiomyopathy (HOCM)
-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
Pulmonary embolus
Prolonged QT
-the QT is more than half the RR
Short QT
-Channelopathy
-Short QT interval (<340ms)
-!!No change in QT with heart rate
-Peaked precordial T waves
-Treatment with AICD
Wolf-Parkinson-White (WPW)
-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!)
WPW
Syncope workup
-!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.)
Hypertensive emergency
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
Hypertensive emergency- 4 end organs
-Heart
-brain
-kidney
-other
Hypertensive emergency- etiology
-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
hypertensive emergency dx
-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)
General targets with IV meds: hypertensive emergency
-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
3 major IV anti-HTN treatment options
-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
Hypertensive emergency: Review on exceptions to the algorithm
-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
A 62yoM presenting via EMS with swelling of his legs and worsening SOB…
37 C, 90bpm, BP 193/118, RR20, O2 94%
Crackles, b/l LE edema, tachypneic
37 C, 90bpm, BP 193/118, RR20, O2 94%
Crackles, b/l LE edema, tachypneic
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.
A 76-year-old man who presented with AMS and then started seizing…
37C, 236/113mmHg, 62bpm, RR14, O2 96%, BG 185mg/dL
37C, 236/113mmHg, 62bpm, RR14, O2 96%, BG 185mg/dL
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.
A 59-year-old woman with known HTN presents to the ED from her PCPs office…
BP is 206/120mmHg
She has no symptoms, did not take her morning medications yet. Exam is normal. Do you want to get any of these?
Labs?
BMP/CBC?
Head CT?
UA?
ECG?
CXR?
IV antihypertensives?
PO antihypertensives?
BP is 206/120mmHg
She has no symptoms, did not take her morning medications yet. Exam is normal. Do you want to get any of these?
Labs?
BMP/CBC?
Head CT?
UA?
ECG?
CXR?
IV antihypertensives?
PO antihypertensives?
NEW TERMS
Severe hypertension
SBP >= 180 mm Hg
DBP >= 110 mm Hg
MAP >=135 mm Hg
Hypertensive emergency
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
Asymptomatic markedly elevated blood pressure (aka severe hypertension)
->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
Documentation
-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.
60 y/o M with dyspnea presenting to the ED late evening
HPI: Patient complained of increasing SOB starting the morning on day of presentation, with a worsening 3 days of non-productive cough. Patient reports no ankle swelling, paroxysmal nocturnal dyspnea, but reports using 2 pillows to elevate himself when sleeping.
No chest pain or other cardiac features. No complaint suggestive of URTI or GI illness. Patient reports no fever, unexplained weight loss or fatigue.
Patient was given Atrovent and Ventolin en route by EMS and was allegedly moving more air into his lungs after this intervention
PMH: chronic back pain, DM, atrial fibrillation, peripheral DM-related ulcers, chronic kidney disease, BPH, colon cancer with hepatic metastases.
PSH significant for 5x CABG, liver and colon resection.
MEDS: Amitriptyline 10mg PO qhs, acetaminophen 650mg PO BID, dutasteride 0.5mg PO daily, ferrous sulfate 300mg PO daily, furosemide 40mg PO BID, metformin 500mg BID, pantoprazole 40mg PO BID, pregabalin 150mg PO BID, primidone 125mg PO daily, rosuvastatin 40mg PO qhs, rivaroxaban 15mg PO daily.
He has a distant 10 pack-years smoking history, drinks alcohol occasionally, and does not use recreational drugs. The patient lives with his wife in their own home.
GENERAL: Pale, non-diaphoretic, tripod position, nebulizer w/ Atrovent and ventolin
VITALS: 36.9C (98.4F), HR 106, RR 22, O2 90% on RA, BP 125/78mmHg.
Cards: Distant S1S2. No JVD. No pedal edema. Cap refill 3s.
Lungs: Basal crackles (right>left), upper anterior lobes with mild wheezing
Abdomen: Soft, NTND
ECG: Sinus tachycardia with LBBB
Labs: Sent off a CBC, CMP, VBG, lactate, BNP
CXR: Ordered, delayed due to staffing
What is your differential so far?
I’m thinking AECOPD vs. congestive heart failure
HPI: Patient complained of increasing SOB starting the morning on day of presentation, with a worsening 3 days of non-productive cough. Patient reports no ankle swelling, paroxysmal nocturnal dyspnea, but reports using 2 pillows to elevate himself when sleeping.
No chest pain or other cardiac features. No complaint suggestive of URTI or GI illness. Patient reports no fever, unexplained weight loss or fatigue.
Patient was given Atrovent and Ventolin en route by EMS and was allegedly moving more air into his lungs after this intervention
PMH: chronic back pain, DM, atrial fibrillation, peripheral DM-related ulcers, chronic kidney disease, BPH, colon cancer with hepatic metastases.
PSH significant for 5x CABG, liver and colon resection.
MEDS: Amitriptyline 10mg PO qhs, acetaminophen 650mg PO BID, dutasteride 0.5mg PO daily, ferrous sulfate 300mg PO daily, furosemide 40mg PO BID, metformin 500mg BID, pantoprazole 40mg PO BID, pregabalin 150mg PO BID, primidone 125mg PO daily, rosuvastatin 40mg PO qhs, rivaroxaban 15mg PO daily.
He has a distant 10 pack-years smoking history, drinks alcohol occasionally, and does not use recreational drugs. The patient lives with his wife in their own home.
GENERAL: Pale, non-diaphoretic, tripod position, nebulizer w/ Atrovent and ventolin
VITALS: 36.9C (98.4F), HR 106, RR 22, O2 90% on RA, BP 125/78mmHg.
Cards: Distant S1S2. No JVD. No pedal edema. Cap refill 3s.
Lungs: Basal crackles (right>left), upper anterior lobes with mild wheezing
ECG: Sinus tachycardia with LBBB
Labs: Sent off a CBC, CMP, VBG, lactate, BNP
CXR: Ordered, delayed due to staffing
What is your differential so far?
I’m thinking AECOPD vs. congestive heart failure
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:
tamponade vs effusion
-RV collapse
61 y/o female with HTN, scleroderma with CREST syndrome (multiple GI complications), ILD, hypothyroidism, GERD, depression, previous pericardial effusion 2015 and bowel resection presenting for back pain and leg pain from sacral and heel decubs. Patient states the pain is worsening over the past 2 days. Also endorses cough with sputum production x 2 days. No palpitations, CP or abdominal pain. No urinary or bowel complaints. No N/V.
Physical Exam
BP 91/64 | Pulse 110 | Temp 97.8 °F (36.6 °C) (Tympanic) | Resp 20
Constitutional: A&Ox3. She appears well-developed and well-nourished. No distress. Smoothed tight skin with fish like facies
Eyes: PERRL.
Neck: Normal range of motion. Neck supple.
Cardiovascular: No murmur heard. Irregular HR
Pulmonary/Chest: Effort normal and breath sounds normal. No respiratory distress. She has no wheezes. She has no rales.
Abdominal: Soft. Bowel sounds are normal. NTND. There is no guarding.
Skin: Skin is warm and dry. Sacral decub stage 2, decub bilateral heels
Patient is mostly bed bound at home. Having difficulty taking care of herself and her disabled son.
Physical Exam
BP 91/64 | Pulse 110 | Temp 97.8 °F (36.6 °C) (Tympanic) | Resp 20
Constitutional: A&Ox3. She appears well-developed and well-nourished. No distress. Smoothed tight skin with fish like facies
Eyes: PERRL.
Neck: Normal range of motion. Neck supple.
Cardiovascular: No murmur heard. Irregular HR
Pulmonary/Chest: Effort normal and breath sounds normal. No respiratory distress. She has no wheezes. She has no rales.
Skin: Skin is warm and dry. Sacral decub stage 2, decub bilateral heels
Patient is mostly bed bound at home. Having difficulty taking care of herself and her disabled son.
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
Patient died
