QI/KT: Hypertension with Drs. Jarrell and Nagel

Epidemiology of Hypertension

30% prevalence in the USA with an increase projected in the future
20% of patients with hypertension are undiagnosed
50% of patients with hypertension are well controlled

Hypertensive Emergency: Elevated BP + End Organ Damage

This usually occurs at BP >180/120 mmHg.

Acute Ischemic Stroke

tPA candidates: goal BP <185/110 mmHg, recommend IV nicardepine or labetalol
Non tPA candidates: treat only if the patient has signs of end organ damage or if BP >220/120 mmHg. If treating, goal is a 10-15% reduction in first hour, recommend IV nicardepine or labetalol

Intracerebral Hemorrhage

ATACH-II trial found no clinical benefit with SBP <140 mmHg
Goal is SBP <160 mmHg in the first hour, recommend IV nicardepine or labetalol

Acute Hypertensive Encephalopathy

Goal is to reduce MAP by 25% over 8 hours, recommend IV esmolol, nicardepine, or labetalol

Acute Coronary Syndrome

STEMI: if considering lytics goal BP <185/110 mmHg, recommend IV or SL nitro with a beta blocker, (IV labetalol, esmolol, or metoprolol)
NSTEMI/UA: if BP >160/110 mmHg, goal is reduce MAP by 20-30%, recommend IV or SL nitro + IV metoprolol

Acute Decompensated Heart Failure

Goal is to reduce SBP by 30 mmHg, recommend IV vasodilators and IV loop diuretics
Caution: SBP lowered to <120 mmHg acutely was associated with adverse outcomes

Aortic Dissection

Goal is SBP 100-120 mmHg and HR 60, recommend IV beta blockers first and then IV vasodilators

Acute Renal Insufficiency (acute decrease in eGFR by >25% from baseline)

Goal is to reduce SBP by no more than 20% within first 2 hours, recommend nicardipine or nitroprusside

Preeclampsia/Eclampsia

Goal is SBP <140 mmHg and goal DBP <90 mmHg, recommend PO nifedepine or IV labetalol. If there is concern for eclampsia treat with magnesium.

Contraindications to beta-blockers: signs of heart failure, evidence of a low-output state, increased risked for cardiogenic shock, or relative contraindications such as heart block, active asthma, or reactive airway disease.

Management of Asymptomatic Hypertension

It is important to consider treatment of hypertension in the ED because improvement in BP control reduces long term rates of stroke and heart disease.

Asymptomatic severe range BP >180/110: ("Hypertensive Urgency" per JNC 7) consider renal panel or UA. If there is no evidence of end organ dysfunction the patient can be discharged but requires out patient follow up.

If the patient has a history of HTN ensure that the patient has adequate BP meds at home.
If the patient is not on any anti-hypertensives consider starting low dose thiazide or CCB (or ACEi/ARB if the patient has CKD) but only after ordering a renal panel.
If patient has a PCP consider reaching out to PCP, with a goal follow up in 1 week.
If the patient does not have a PCP, refer to primary care.

Asymptomatic BP >140/90: patients do not need routine work up in the ED beyond a history and physical exam.

If the patient is already being treated for hypertension ensure that the patient has adequate BP meds at home.
It is important to review the patient's chart to see if they have had elevate BPs in the past, if so consider starting a thiazide or CCB (or ACEi/ARB if the patient has CKD) but only after ordering a renal panel.
If patient has a PCP consider reaching out to PCP, with a goal follow up in 1 month.
If the patient does not have a PCP, refer to primary care.

Do not attempt to normalize asymptomatic hypertension in the ED. Please inform the patient that their blood pressure is elevated and provide appropriate discharge instructions. Please include information about the DASH diet in the discharge instructions.

R4 Sim: Endocarditis and Acute Aortic Insufficiency with Drs. Gorder, Lagasse, O'Brien and Polsinelli

Acute Severe Aortic Regurgitation due to Aortic Valve Endocarditis

History: Patient is a male in his 30s with a pmhx of IVDU who presents with chest pain and shortness of breath. The patient states that he has had chest pain, trouble breathing, back pain, and subjective fevers over the past week. He describes the chest pain as exertional. He also admits to bilateral leg swelling and orthopnea. No medications or allergies.

Vitals: HR 135 BP 104/82 RR 32 SpO2 91% on RA Temp 100.7F

Exam: +JVD, tachypnea with bibasilar rales, tachycardia with a regular rhythm, +S3 gallop, weak peripheral pulses, a high-pitched blowing diastolic murmur, and 2+ symmetrical bilateral lower extremity pretibial pitting edema to the level of the knee

EKG: Sinus tachycardia with LVH

CXR: Pulmonary edema

Labs: Significant for leukocytosis, anemia, acute kidney injury, elevated lactate, elevated troponin and BNP, and elevated LFTs.

Causes of Acute Aortic Regurgitation:

Endocarditis (valve destruction, leaflet perforation, perivalvular abscess rupturing into the L ventricle)
Aortic dissection into the valve (Sanford Type A)
Trauma (usually deceleration injuries)
Iatrogenic (s/p TAVR, etc.)
Mechanical valve/prosthesis problems

Dissection and endocarditis are by far the two most common causes of acute AR.

Pathophysiology:

Problem occurs with aortic valve causing acute AR
Left ventricle cannot increase stroke volume as it does not have time to increase end-diastolic volume like in chronic AR
LVEDP rises
Mitral regurgitation will then occur
This causes elevated left atrial and pulmonary venous pressures, leading to pulmonary edema
You will see hypotension (decreased CO) with narrow pulse pressure (increased SVR)

Physical Exam:

Patients with severe AR will often show signs of cardiac shock (cyanosis, cool extremities, pallor)
If aortic dissection is the cause, you may see findings on exam consistent with this (unequal pulses, etc.)
Look for JVD, crackles/rales, hepatomegaly
Patients will often have a loud S3 and an early diastolic rumble

Diagnostics:

EKG will usually show sinus tachycardia
CXR may show nothing, or may show pulmonary edema. If the cause is due to dissection, you may see a widened mediastinum or a hemothorax
Echocardiogram is the test of choice
- Doppler is used to show the regurgitation
- In severe cases, end-diastolic velocity in the LV is essentially zero, as the aortic diastolic pressure and the LVEDP are equal
CT can be used if the physician is concerned about dissection as an etiology

Treatment:

For cases of severe acute aortic regurgitation, the treatment of choice is emergent valve replacement
Vasodilator therapy is indicated for emergent afterload reduction with the goal of decreasing LVDEP; nitroprusside is the drug of choice (unless the etiology is aortic dissection)
Dobutamine would be the pressor of choice due to its inotropy and possibility of increasing forward flow and lowering LVEDP

Quick Hit Murmurs

Murmur Basics:

Murmurs are due to nonlaminar flow through an anatomic structure
S1: closure of the mitral and tricuspid valves
S2: closure of the aortic and pulmonic valves
Between S1 and S2 is systole, ventricular ejection
Between S2 and S1 is diastole, ventricular filling
Describing murmurs: timing (systolic, diastolic, or continuous), pitch, intensity (graded 1-6), contour (crescendo vs decrescendo), radiation, and dynamic changes- response to maneuvers

Aortic Stenosis:

Harsh systolic ejection murmur, best heard at the right second intercostal space, radiating to the carotids
Most commonly caused by degenerative calcification (calcified aortic stenosis) in the USA, most commonly caused by rheumatic heart disease world wide
Pathophysiology: obstruction of LV outflow due to stenosis of the aortic valve causes LV hypertrophy. Eventually this impairs diastolic filling and CO decreases, impairing systemic and coronary blood flow.
Symptoms: (classic triad) dyspnea, chest pain and syncope, but many people are asymptomatic for long periods of time
Management: medications that reduce inotropy (BB, CCB) and drugs that reduce preload or afterload are poorly tolerated (vasodilators, NTG, diuretics) as patients are preload dependant
Beware of afib as this reduces preload in these patients. Patients may require cardioversion to restore normal sinus rhythm and optimize preload
Patients presenting with symptomatic aortic stenosis should be admitted for further management

Mitral Regurgitation:

Holosystolic murmur with a clear S2
Acute presentations of mitral regurgitation can be caused by papillary muscle or chordae tendinae rupture from an MI. Other causes include valve leaf perforation from endocarditis, and rarely from blunt thoracic trauma
- When mitral regurgitation occurs acutely patients can present with pulmonary and peripheral edema. In severe case patient can have cardiogenic shock from a lack of forward blood flow and loss of CO
- Acute treatment: stabilize, PCI if indicated, and emergent cardiology and cardiac surgery consultation
Chronic presentations can be caused by mitral valve prolapse or more commonly by fibroelastic deficiency syndrome in the elderly. This is usually a progressive disease, causing progressive DOE and afib due to LA dilation

Aortic Regurgitation:

High pitched blowing diastolic murmur heard immediately after S2 that is loudest at the left sternal border
Pathophysiology: aortic regurgitation occurs when valve leaflets fail to close fully, causing blood to flow from the aorta into the LV during diastole. Acutely, this causes an increase in LV pressure causing mitral regurgitation and pulmonary congestion.
Symptoms: tachycardia, tachypnea, respiratory distress
Etiologies:
- Valvular causes: most commonly endocarditis, bicuspid aortic valves, rheumatic disease
- Non valvular causes: most commonly aortic dissection, blunt chest trauma
Diagnosis is made on ECHO
Management: acute aortic regurgitation requires immediate surgical intervention
- Want to augment forward flow and reduce LVEDP- can use nitroprusside combined with inotropic agents such as dobutamine
- Diuretics and nitrates are usually ineffective
- Avoid BB because they block the compensatory tachycardia that is critical in maintaining CO

Evaluation of a New Murmur in the ED

Patients that require admission and further work up:

Any new diastolic murmur
Patients who are symptomatic from their murmur ex. chest pain, syncope, DOE, SOB, lower extremity edema, new O2 requirement
Patient with abnormal CXR or EKG

Global Health Quick Hits with Dr. Bryant

Travel history: The Devil's in the details

Have you traveled outside of the US? When did you return? How long after you left did your symptoms begin? Did you receive any vaccines and or take prophylaxis? It is also important to ask about accommodations, water exposure, insect precautions or bites, animal exposure or bites, medical care abroad, and body fluid exposure.

Case 1. 22 yo F with 6 weeks of dysuria and hematuria

The patient complains of pink tinged urine for the past 6 weeks and dysuria most notable at the end of urination. The patient has had a very through work up at an outside hospital prior to today's ED visit including blood and urine cultures that were negative, BMP, CBC, and non contrasted CT of her abdomen and pelvic which was normal. Patient recently traveled to North Africa.

Repeat UA was significant for gross hematuria. The urine is spun down and evaluated under the microscope.

Schistosomiasis

Most common cause of hematuria worldwide
Treatment: Praziquantal
Follow up: Urology, chronic infections are at high risk of bladder cancer

Case 2: 30 yo M with rash and bug bite

Patient has had no fevers but rash has been very painful. Completed an outpatient course of bactrim and keflex without improvement in symptoms. Recent travel to Belize. Physical exam reveals raised, mildly erythematous single lesion on the scalp associated with localized hair loss.

Botfly

8 week life cycle of the larva which are obligate anaerobes.
Treatment: Removal of larva with local anesthesia

Case 3: 32 yo F with headache and dizziness

Complains of intermittent nausea and headache. No previous history of headaches. CT head revealed oviod cyst at grey white junction.

Neurocysticercosis

Most common parasitic CNS infection and most common acquired cause of epilepsy world wide.
Workup: CBC for eosinophilia, needs LP
Treatment: Albendazole

R1 Clinical Diagnostics: Procalcitonin with Dr. Lane

See Dr. Lane's Primer on Procalcitonin

Pediatric Population

Procalcitonin is commonly used in pediatric practice. Recently described in 2016 in Pediatrics, the "step-by-step" method discusses the use of procalcitonin in the risk stratification of serious bacterial illness (SBI) in the febrile infant. This has been prospectively validated and has found to be superior to the Rochester criteria and the Lab-score.

Case 1: 72 yo F with pmhx of HTN, HLD, DM2, and recent UTIs presents with altered mental status

Patients who have a procalcitonin value greater than 2 ng/mL were found to be at higher risk for gram negative bacteremia.

MOSES study showed that an inability to decrease procalcitonin levels by 80% between ICU day 1 and 4 was found to be an independent predictor of mortality.

Case 2: 68 yo M with HTN presents with cough and fever found to be tachypneic and hypoxic with asymmetric lung sounds

Mixed evidence exists about the use of procalcitonin for the diagnosis and/or management of sepsis. However, current sepsis guidelines do mention the consideration of procalcitonin in deciding length of antibiotic therapy.

Case 3: 49 yo F with presents with 2 weeks of productive cough and fevers

An isolated day 0 procalcitonin does not improve the ability to predict mortality in patients with pneumonia.

ProHOSP RCT trial showed that procalcitonin can be potentially used to help guide discontinuation of antibiotics in patients with lower respiratory tract infections.

Pitfalls

Any inflammatory state can cause an increase in procalcitonin.
ESRD impairs clearance of procalcitonin.
At extrememly high levels, procalcitonin can be read as falsely low without serial dilution

CPC with Drs. Habib and Roche

Case: The husband of a woman in her 70s calls 911 because his wife suddenly became unresponsive. The husband was concerned that the wife had a cardiac arrest and preformed CPR. EMS evaluated the patient and palpated a pulse but found the patient to have a GCS 3. The patient was intubated by EMS for airway protection.

The patient has a pmhx of afib on coumadin, DM, history of previous stroke, and HTN. In the ED the patient is noted to be intubated, with mild crackles on pulmonary exam, and is minimally responsive with GCS 3. EKG is notable for afib. CXR shows mild pulmonary edema.

Imaging: non contrasted head was negative for ICH. CT angiography of the chest, abdomen, and pelvis did not show PE, AAA, or dissection

Differential diagnosis of sudden unresponsiveness with questionable cardiac arrest:

Terminal dysrhythmia- VT or VF possibly due to acute coronary syndrome or hyperkalemia
STEMI
Aortic catastrophe- possibly due to dissection, AAA
Massive PE
Stroke- possibly basilar occlusion
Seizure- non convulsive status, prolonged postical, non convulsive status
Hypoglycemia

Dr. Roche's Guess: CT Angiography Head and Neck for Basilar Artery occlusion

Test of choice: CT Angiography Head and Neck
Diagnosis: Basilar Artery occlusion

Basilar Artery Occlusion & Posterior Circulation Stroke

20% of all strokes involve the posterior circulation. Posterior circulation strokes most commonly involve the vertebral artery.
5 D's of posterior strokes: dizzy, diplopia, dyasrthia, dysphasia, and dystaxia
Symptoms: commonly present with headache, dizziness or vertigo, nausea and vomiting

Basilar Artery Syndromes: 14% of posterior strokes, typically intrinsic occulsive disease, often involving the pons with devestating symptoms

Locked in Syndrome: paralysis of the limbs and facial structures. Vertical gaze is often preserved.

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