#truelearn

Knee Ligaments Review

Ottawa knee rules are less sensitive in children; use Pittsburgh rules to determine whether or not to obtain radiographs

MRI is 95% and 90% accurate in identifying ACL tears and meniscal injuries, respectively

Pain with varus or valgus stress is more suggestive of ligament damage than a meniscus tear

The MCL is the primary static stabilizer against valgus stress at the knee

The LCL is the primary static stabilizer against varus stress at the knee

The ACL is the primary static stabilizer of the knee against anterior translation of the tibia with respect to the femur

The PCL is the primary static stabilizer of the knee against posterior translation of the tibia with respect to the femur

WB, NWB = weight bearing or non weight bearing

Ligament injuries are graded as follows:

Grade 1: stretching of the ligament with no detectable instability

Grade 2: further stretching of the ligament with detectable instability, but with the fibers in continuity

Grade 3: complete disruption of the ligament.

Meniscal Tear

Acute: Twisting injury on weight bearing knee

Chronic: degenerative tears, mechanical grinding of osteophytes on meniscus

Late teens, peak (30-40)

MC: medial meniscus

HX:

1. Foot planted with femur rotated internally with valgus stress (medial) OR

2. Femur rotated externally with varus stress (lateral)

1. Most acute tears (younger pt) are vertical longitudinal or oblique tears

2. Complex and degenerative tears (older pt)

HX: axial loading with rotation or HX of osteoarthritis

1. Pain (variable)

-Event followed by insidious pain and swelling over 24 hours

-Worse with twisting or pivoting

-Mechanical SX: ”Tearing” or “popping” sensation: popping, locking, catching, or “knee giving out”; cannot extend fully

2. Effusion (common) -patient will complain of stiffness  

Signs

1. Joint line tenderness (sensitive, non specific)

2. Abnormal ROM: loss of smooth passive motion or full extension

-Locking, instability  

3. Inability to squat or kneel; can bear weight

4. Joint effusion

1. McMurray Maneuver: catching, pop, or click at joint line

2. Flexion McMurray: pain over posteromedial joint line

3. Apley grind test: pain at either joint line

4. Thessaly Test: shows pain

Imaging

1. X-ray of knee: degeneration, calcification

2. MRI - most sensitive (confirm)

1. Rest, ice for 15 mins every 4-6 hours, elevate, crutches, patellar restraining brace

2. Steroid injection - only useful if patient has OA complicated by meniscal tear

3. Surgery if mechanical symptoms present

-Arthroscopy

-If small <15 mm: heals spontaneously

-Repair larger tears

(a) Partial meniscectomy: short recovery

(b) Repair rather than meniscectomy (esp in young)

Health Maintenance

1. Tears that occur centrally have a longer healing rate

2. Return to full function may be expected in 6–8 weeks

3. High risk of OA if meniscectomy at young age

Anterior Cruciate Ligament (ACL) Tear

Occur with sudden deceleration with a rotational maneuver, usually without contact; OR contact injury with valgus force to extended knee

F > M

Associated: high incidence of lateral meniscal tears

HX: hyperextension and/or valgus force to knee by direct blow

1. “Pop” reported by patient

2.  Knee swelling within 4-12 hours of injury

Signs

1. Unable to fully bear weight (instability), knee giving out with twisting activities

2.

1. Lachman Test

-Most sensitive for diagnosis

2. Anterior Drawer Test

3. Pivot Shift Test: helps evaluate rotational instability

Imaging

1. XR: normal

2. MRI (confirms)

1. Supportive

-Pain relief with Tylenol +/- NSAID

-Limit ROM, place in long leg brace

-Obtain XR if indicated

-Consider MRI

2. Refer to Ortho

-Surgical repair once full ROM obtained

-Double-bundle reconstruction

-RTA in 4-6 months

-Physical therapy

Lateral Collateral Ligament (LCL) Injuries

“Knee buckling” into hyperextension with normal gait ‘

Associated: peroneal nerve injury (12-29%)

1. HX: valgus/varus stress to extended knee

2. Pain over lateral aspect of knee joint

3. Hemarthrosis

Signs

1. Able to bear weight without instability or locking

2. Laxity with varus stress testing with knee at 30 degrees flexion

3. Tenderness along lateral joint line

4. Neurovascular exam: r/o peroneal nerve injury

5. Dial test: most useful to evaluate for posterolateral instability

1. XR: normal or fibular head avulsions, patellar dislocation, loose bodies; lateral joint space narrowing with osteophytes and subchondral sclerosis

2. MRI: abnormal

1. Supportive

-Pain relief with Tylenol +/- NSAID

-Limit ROM, place in long leg brace

-Obtain XR if indicated

-Consider MRI

2. Refer to Ortho

-All start early PT

-Grade I: 2-4 weeks immobilization → Quad strengthening

-Grade II: brace blocking last 20 degrees of flexion, WBAT

-Grade III: surgery

Health Maintenance

1. Limit weight bearing after surgery for 6 weeks, brace for at least 3 weeks

Medial Collateral Ligament (MCL) Injuries

MCL is primary restraint to valgus stress, attached to medial meniscus at joint line

Forced abduction of leg at knee

Associated: tear of medial meniscus and rupture of ACL (look for immediate swelling)

1. HX twisting injury or direct blow at knee with valgus strain

2. Pain over medial aspect of knee joint

3. Joint effusion if severe

Signs

1. Medial joint line tenderness

2. Patellar apprehension test

-Check for patellar dislocation

3. Laxity to valgus stress at 30 degrees of flexion

1. XR: not helpful unless made with valgus stress applied

2. MRI - r/o concomitant meniscal injury (confirms)

1. Supportive

-Pain relief with Tylenol +/- NSAID

-Limit ROM, place in long leg brace

-Obtain XR if indicated

-Consider MRI

2. Refer to Ortho

-All start early PT

-Grade I: WBAT, early amb

-Grade II: brace blocking last 20 degrees of flexion, WBAT

-Grade III: hinged brace, initial NWB, advance WB over 4 weeks

Posterior Cruciate Ligament (PCL) Tear

Most common mechanism of injury: direct blow to anterior tibia with knee flexed or fall to ground with foot plantar flexed

Associated: posterolateral corner (meniscus) tear (60%)

1. Knee pain

- Biggest complaint

2. Swelling

3. Stiffness

Signs

1. Abrasions or ecchymosis around proximal anterior tibia

2. Ecchymosis in popliteal fossa

3. Instability

1. Posterior Drawer Test

2. Posterior Sag (Godfrey) Test

3. Reverse Pivot Test

Imaging

1. MRI

1. Non-surgical

-Obtain full quad strength

-Grade I/II: early motion, WBAT

-Grade III: keep knee immobilized in extension

-Surgery to prevent osteoarthritis or instability

Health Maintenance

1. Bracing is ineffective

2. Minimum 3 months rehab before return to play  

Thessaly Test: have patient hold your hand and have patient stand on one leg with knee flexed to 20 degrees, then patient will internally and externally rotate their knee

Pain or locking/catching sensation = (+) test, 90% sensitive, 96% specific

McMurray Test: repeated passive flexion and extension of knee; painful click in early or mid extension of the knee = meniscal tear

Grasp patient’s heel with one hand and place fingers and thumb of other hand along joint line; passively flex knee and internally rotate tibia; extend the knee while maintaining internal rotation; passively flex the knee while externally rotating

Sensitivity: 50%, specificity 60-97%

Apley Test: patient prone with affected knee flexed 90 degrees, stabilize thigh with a knee or hand; press patient’s heel toward the floor while internally and externally rotating the foot; pain = (+) test

Sensitivity: 38-41%

Lachman Test: Knee flexed at 20 degrees, stabilizing the distal femur with one hand and pulling forward on the proximal tibia with the other hand

Anterior Drawer Test: With the patient supine and the knee flexed to 90 degrees (hip flexed to about 45 degrees), the foot is restrained by sitting on it and the examiner's hands are placed around the proximal tibia. Then, while the hamstrings are felt to relax and the tibia is pulled forward, the displacement and the end point are evaluated.

Pivot Shift (Losee) Test: a valgus and internal rotation force is applied to the tibia; Starting at 45 degrees of flexion, the lateral tibial plateau is reduced. Extending the knee causes the lateral plateau to subluxate anteriorly with a thud at about 20 degrees of flexion. It reduces quietly at full extension

Posterior Drawer Test: The posterior drawer test evaluates the integrity of the PCL. It is performed with posterior pressure on the proximal tibia with the knee flexed at 90 degrees and

Posterior Sag (Godfrey) Test: This test involves flexing the knee and hip and noting the posterior pull of gravity creating posterior “sag” of the tibia on the femur

Dial Test: externally rotate each tibia and note the angle subtended between the thigh and the foot. The dial test is performed at 30 and 90 degrees of flexion with a significant difference being an angle 5 degrees or greater than the contralateral leg. Injury to the posterolateral capsule alone is confirmed with greater external rotation at 30 degrees, an isolated PCL at 90 degrees, and to both structures when there is greater rotation at 30 and 90 degrees compared to the uninjured leg

Obtain X-ray for:

Ottawa Knee Rules

Sensitive

Pittsburg Knee Rules

Greater specificity

1. Age >55

2. Tenderness to head of fibula

3. Isolated tenderness to patella

4. Inability to flex knee to 90 degrees

5. Inability to bear weight for 4 steps both immediately and in examination room regardless of limp

1. Recent fall or blunt trauma

2. Age <12 y/o or >50 y/o

3. Unable to take 4 unaided steps

Please enjoy these free TrueLearn questions below and check out the link above for more!

Question 1: A 40-year-old man presents to the office complaining of right knee pain for the past three days after a weekend football game in his neighborhood. He fell with his knee in extension after being tackled and felt a sudden sharp pain as he hit the ground. Afterwards, he could not stand on the knee and has been taking acetaminophen and using ice packs to help reduce the swelling. He is in moderate pain and cannot walk up and down stairs in his house. On examination, the right knee is red and swollen with a mild effusion anteriorly. The left knee appears normal. There is mild tenderness to palpation diffusely. There are no sites of penetration or fluctuance. A Lachman’s test is positive. Which of the following is the most likely diagnosis for this patient?

Anterior cruciate ligament injury

Lateral collateral ligament injury

Medial collateral ligament injury

Medial meniscus injury

Posterior cruciate ligament injury

Explanation:

The most common set of knee injuries are the anterior cruciate ligament (ACL), medial collateral ligament (MCL), and medial meniscus (the unhappy triad of knee injuries). The ACL provides anterior stability to the knee and is injured in periods of hyperextension. It originates at the posteromedial aspect of the lateral femoral condyle and courses in an anterior and medial fashion to the anteromedial aspect of the tibia between the condyles, as shown below. Patients report a sharp sudden pain as the ligament is torn. The Lachman’s test is specifically designed to evaluate the anterior cruciate ligament. During the test, a patient lays supine with the knee flexed at 20º while the examiner pulls anteriorly with the tibia and stabilizes the femur. The anterior drawer sign can also be used to evaluate ACL injury as the patient lays supine with the knee flexed at 90º and the hips flexed at 45º. The examiner pulls the tibia forward and, similar to the Lachman’s test, will note hypermobility anteriorly if there is an injury.

Answer B: The lateral collateral ligament can be examined with Varus stress on the knee. If damaged, the physician will note hyperlaxity with the stress.

Answer C: A medial collateral ligament injury can be diagnosed with Valgus stress and injury is noted if there is hyperlaxity in relation to the medial aspect of the knee.

Answer D: The medial meniscus can be evaluated by the McMurray’s test. The patient lies flat and the examiner flexes the knee. A click may be felt on the medial joint line. Then, the foot is torqued medially as the knee is rotated laterally in order to trap the meniscus and note further pain and clicking. The directions can be reversed for evaluating the lateral meniscus.

Answer E: The posterior drawer sign can be elicited to evaluate for a posterior cruciate ligament injury. The knee is flexed at 90º with the hips flexed at 45º as the tibia is pushed posteriorly against a fixed femur. Posterior hyperlaxity will be noted if there is an injury.

Bottom Line: The ACL tear is one of the most common knee injuries and can be diagnosed by the Lachman’s and anterior drawer tests. Treatment is surgical if the patient intends to return to the sport or strenuous activities. The following links are some videos to help with understanding the various physical exam maneuvers for diagnosing knee injuries.

*McMurray: http://www.youtube.com/watch?v=fkt1TOn1UfI

*Lachman’s test: http://www.youtube.com/watch?v=dH_jnTy1rNk

*Anterior Drawer Test: http://www.youtube.com/watch?v=yQdBrr3Mmj0

For more information, see:

Anterior Cruciate Ligament Injury on Medscape

Question 2: A 39-year-old male presents to the office with the complaint of left knee pain and swelling for five days' duration. He denies fevers, chills, or other joint involvement. History reveals the presence of locking and popping in the left knee that began while playing flag football. At this time, he felt a pop and had immediate pain and swelling. The symptoms initially improved with ice, then became more painful. Physical examination reveals the left knee is warm to the touch, swollen, and very tender to palpation along the joint line. Further examination reveals a positive McMurray test. The most appropriate test to confirm the diagnosis is a

bone scan of the lower extremity

computed tomography with contrast of the lower extremity

magnetic resonance imaging of the lower extremity

ultrasound of the lower extremity

radiograph of the lower extremity

Explanation:

This patient is suffering from a torn meniscus. The medial meniscus is torn three times more commonly than the lateral meniscus. However, when the ACL is torn, the lateral meniscus is more commonly involved, such as in the terrible triad of the knee (ACL, MCL and lateral meniscus). Traumatic meniscal tears occur more commonly in young, athletic adults, while degenerative meniscal tears occur more often in older patients. Meniscal injuries are typically due to a twisting moment about the knee while it is under load, such as when a football player makes a turn while running. The McMurray test recreates the forces that cause the tear. This is done by having the patient supine with the affected knee flexed to 90 degrees with a valgus stress applied, then externally rotating and extending the knee. A positive test is indicated by pain or a “click”. The diagnostic test of choice is a magnetic resonance imaging (MRI). MRI is the test of choice for ligament injuries, meniscal disease, avascular necrosis, and articular cartilage defects of the knee.

Answer A: Bone scans are useful in diagnosing stress fractures, but not particularly helpful for meniscal tears.

Answer B: Computed tomography (CT) scans have been largely replaced by MRI for the evaluation of soft tissue structures, such as the fibrocartilage in the meniscus. Though, they remain useful for the evaluation of bony tumors and fractures.

Answer D: Ultrasound is beneficial for evaluating soft tissue lesions about the knee, such as patellar tendonitis, hematomas and extensor tendon ruptures.

Answer E: Radiographs are an initial diagnostic modality that will be performed to rule out bony injury, however they will not provide the soft tissue imagery necessary to diagnose a torn meniscus.

Bottom Line: An MRI is the diagnostic study of choice to evaluate meniscal injuries of the knee. For more information, see: Ayala C, Spellberg B. Boards and Wards. 4th Ed. Philadelphia, PA; Lippincott Williams & Wilkins; 2010: 201. Le T, Bhushan V, Skapik J, et al. First Aid for the USMLE Step II 2007: A Student-to-Student Guide. New York, NY: McGraw-Hill; 2007: 245 "Meniscal Injuries" on Medscape. http://emedicine.medscape.com/article/308054-overview. "Meniscal injury of the knee" on UpToDate. http://www.uptodate.com/contents/meniscal-injury-of-the-knee. Miller MD, Thompson SR, Hart JA, et al. Review of Orthopaedics. Philadelphia, PA: Elseiver-Saunders; 2012: 294 Updated: September 19, 2012

Question 3: A 35-year-old man complains of a painful and swollen right knee that began after playing ice hockey three days ago. He fell on his knee during the game and had difficulty playing the rest of the game. He has had severe difficulty walking down stairs for the last three days and has been using ice packs frequently to help reduce the swelling. He denies any fever or chills. His medical history is only significant for a splenectomy after being involved in a car accident 10 years ago. On examination, the entire right knee is edematous in comparison to the left, without erythema or warmth. There is tenderness to palpation of the medial side of the knee and valgus stress causes pain and increased motion at the knee joint. Which of the following is the most important step in managing this patient?

Corticosteroids

Immobilization and observation

Joint fluid aspiration

MRI of the knee

X-ray of the knee

Explanation:

This patient with a history of trauma and pain on palpation on the medial aspect of the knee most likely has a medial collateral ligament tear. The medial collateral ligament is part of the “unhappy triad” (anterior collateral ligament, medial meniscus, and medial collateral ligament) most commonly injured in knee trauma. These structures are most commonly injured because knee injuries occur most commonly following valgus stress. In order to visualize the soft tissue structures of a knee, patients require an MRI. The MRI will show the ligaments and reveal any tears.

Answer A: Patients with chronic arthritis may require corticosteroid injections. Patients should not receive more than one injection per month for seriously affected joints. This plays no role in treatment of an acute injury due to trauma.

Answer B: Immobilization would not be best because a diagnosis has not been made. Many medial collateral ligament injuries are partial tears and will require an immobilizer brace, but this should only be utilized if the diagnosis is confirmed by imaging.

Answer C: Joint fluid aspiration is utilized for infected joints. Although this joint is swollen, it is not fluctuant or warm. Though a history of splenectomy may suggest a higher risk for infection, this patient does not exhibit the classic signs or symptoms of a septic joint. This patient has a known traumatic incident, not an infectious etiology from a puncture or systemic infection.

Answer E: An x-ray is useful for evaluating any breaks or osteoarthritis but not for visualizing the ligaments.

Bottom Line: Medial collateral ligaments are commonly injured and present with pain on palpation of the medial side and hyper-laxity of the joint with valgus stress due to increased instability.

Asthma

Pulmonology makes up 12% of the PANCE and between 10-15% of the End of Rotation Examinations. This means that topics like Asthma, which are found on every topic blueprint, are likely to pop up. This makes it essential for you to know the ins-and-outs of asthma treatment plans, including triggers, signs and symptoms, diagnostic studies, severity index, and stepwise therapy.  

Before we begin, I want to point you in the right direction. Check out the guidelines by the NIH and the National Asthma Education and Prevention Program (NAEPP), which most PA schools teach.

Asthma Quick Care Reference

Guidelines for the Diagnosis and Management of Asthma

Asthma Action Plan (English) (Spanish)

Asthma and Physical Activity in the School

Parent Handout for a Child with Asthma

Managing Asthma: A Handout for Schools

And don't forget, for more practice questions, visit TrueLearn.com/DoseOfPA

Now onto the basics of Asthma...

Characteristics

Airway inflammation

Airway hyperresponsiveness

Reversible airflow obstruction

May begin at any age

Dyspnea common when exposed to rapid changes in temperature and humidity

Extrinsic

Intrinsic

Atopic: produce IgE to environmental triggers (eczema, hay fever)

Become asthmatic at young age

Not related to atopy or environmental triggers

PFTs (obstructive): decreased expiratory flow, low FEV1, and decreased FEV1/FVC ratio

Increased FEV1 > 12% with albuterol

Decrease in FEV1 >20% with methacholine or histamine

Increase in diffusion capacity of lung for carbon monoxide (DLCO)

General

Signs and Symptoms

Diagnostics

Therapy 1

Therapy 2

Triggers: pollens, house dust, molds, cockroaches, cats, dogs, cold air, viral infections, tobacco smoke, meds (BB, aspirin), exercise

Intermittent: SOB, wheezing, chest tightness, cough

-Occurs in 30 mins to exposure to triggers

-Symptoms worse at night

-Wheezing (inspiration AND expiration) is most common finding

-CXR: for first time wheezers

-PFTs: required to DX

-Spirometry before and after bronchodilators: increase in FEV1 or FVC by 12%

-SABA (albuterol) for acute attacks

Onset 2-5 min, duration is 4-6 hours

-LABA (salmeterol) for nighttime asthma and exercise induced asthma

-Inhaled Corticosteroids: mod to severe asthma

Use regularly to decrease airway hyperresponsiveness and exacerbations

-Montelukast: prophylaxis for mild exercise induced asthma and control of mild-mod

Allows for reduction in steroid and B2

-Cromolyn sodium: prophylaxis before exercise

AVOID Beta-BLOCKERS in asthmatics

Acute Asthma Exacerbation

Tachypnea

Sweating, wheezing, speaking in incomplete sentences, use of accessory muscles

-Paradoxical movement of the abdomen and diaphragm on inspiration

-Peak exp flow: low

Severe <60

-ABG: increased A-a gradient

-CXR: r/o pneumonia, pneumothorax

-Inhaled B2 agonist via nebs or MDI

-Corticosteroids: IV or orally

-IV magnesium: can help prevent bronchospasm

Complications:

-Status asthmaticus: does not respond to standard meds

-ARDS: resp muscle fatigue

-Pneumothorax, atelectasis, pneumomediastinum

Monitor peak flow (peak expiratory flow rate) - measures airflow obstruction

Adult normal ranges: 450-650 L/min (men) vs. 350-500 L/min (women)

Mild >300, Mod-Severe 100-300, Severe <100

Mild persistent asthma: monitor periodically, increase dose of inhaled steroid if peak flow decreases

Moderate persistent asthma: daily monitoring required. Increase dose of inhaled steroid if peak flow decreases

Severe persistent: daily monitoring; initiate prednisone if peak flow decreases

Severity

Long-term Control Medications

Mild intermittent (symptoms <=2 times/week)

None

Mild persistent (symptoms 2+ times/week, not everyday)

Low dose inhaled corticosteroid

Moderate persistent (daily sx, frequent exacerbation)

Daily inhaled corticosteroid (med dose) or cromolyn/nedocromil, methylxanthine, or antileukotriene

Severe persistent (continued sx, frequent exacerbation, limited physical activity)

Daily corticosteroid (high dose)

+ LABA or methylxanthine

+ oral corticosteroids

Bronchoprovocation test - useful when asthma suspected, but PFTs non-diagnostic

Measures lung function before and after inhalation of increasing doses of methacholine; hyperresponsive airways → obstruction at low doses

Chest XR - severe asthma reveals hyperinflation

Only get with severe asthma to r/o pneumonia, pneumothorax, pneumomediastinum, foreign body

Arterial Blood Gas (ABG) - if significant respiratory distress

Hypocarbia (common) with hypoxemia

If PaCO2 normal or increased, respiratory failure may ensue - asthmatics have increased respiratory rate, which should cause PaCO2 to DECREASE

Treatment

Acute Mild

PEF ≥ 70% pred or best

Dyspnea only with activity

SABA x 1-2 puffs (spacer, VHC, nebulizer)

First time wheezing – chest x-ray

Possible short course oral steroids

SABA prn: Albuterol

Acute Moderate

FEV1/PEF 40-69% pred or best

Dyspnea with normal activity

Requires office or ED visit

SABA x q 20 min (VHC, nebulizer) – 1 hr

SABA x q 60 min – 3 hrs; decide admit

Oral steroids

O2 if needed (SaO2 ≥ 90%)

Low dose inhaled corticosteroid: Fluticasone (Flovent)

Acute Severe

FEV1/PEF <40% pred or best

Dyspnea with conversation

Requires ED/hospitalization

High dose SABA (VHC) + anticholinergic (nebulizer, MDI) x q 20 min – up to 4 hr

Systemic Steroids – PO or IV

O2 if needed (SaO2 ≥ 90%)

Low dose ICS + LABA : Advair + Symbicort

Medium dose ICS + LABA

Advair or Symbicort

Life-Threatening

PEF <25% pred or best

Too dyspneic to speak

Requires ED/hospitalization/ICU

Possible Intubation and Mechanical Ventilation

Treatment as above; hourly/continuous SABA

IV Systemic Steroids

O2 if needed (SaO2 ≥ 90%)

High dose ICS + LABA + oral steroids

Advair or Symbicort + Prednisone

Sample Questions Provided by TrueLearn

Question 1: A 16 year old female presents to the ER in severe respiratory distress. She complains of persistent cough, dyspnea and chest tightness. Physical exam reveals a decreased inspiratory to expiratory duration, accessory muscle use, tachypnea, tachycardia, and decreased breath sounds. Upon further auscultation you hear the breath sound in the exhibit. What is the best next step in management of this patient’s condition?

Montelukast

Zafirlukast

Cromolyn

Albuterol

Theophylline

Explanation:The most likely diagnosis is asthma. Asthma is a reversible airway obstruction secondary to bronchial hyperreactivity, airway inflammation, mucous plugging and smooth muscle hypertrophy. Patients often present with cough, episodic wheezing, dyspnea, and chest tightness. Symptoms often worsen at night or early in the morning. Physical exam reveals wheezing, prolonged expiratory duration (decreased inspiratory to expiratory ratio), accessory muscle use, tachypnea, tachycardia, decreased breath sounds (late sign), decreased oxygen saturation (late sign), hyperresonance and possible pulsus paradoxus. Arterial blood gases demonstrate mild hypoxia and respiratory alkalosis. Normalizing PCO2, respiratory acidosis and more severe hypoxia in an acute exacerbation warrant close observation as they may indicate fatigue and impending respiratory failure. Spirometry may show a decreased FEV1/FVC ratio. Eosinophilia may be seen on a CBC while a CXR shows signs of hyperinflation. Asthma can be definitively diagnosed with a methacholine challenge test. Treatment in general includes avoiding allergens and potential triggers, beta-2 agonists, corticosteroids, muscarinic antagonists, methylxanthines, cromolyn and antileukotrienes. Treatment is dependent on classification. Asthma is divided into 4 types: mild intermittent, mild persistent, moderate persistent and severe persistent. Acute treatment of an asthma attack involves supplemental oxygen, bronchodilators such as albuterol and muscurinic antagonists such as ipratropium.

Answers A & B: Montelukast and zafirlukast are antileukotrienes that work by blocking leukotriene receptors thereby preventing bronchoconstriction. Zileuton is a 5-lipoxygenase inhibitor that blocks the conversion of arachidonic acid to leukotrienes thereby blocking bronchoconstriction. These medicines are not used in the acute treatment of asthma, they are used to prevent asthma attacks.

Answer C: Cromolyn prevents the release of vasoactive mediators from mast cells. It is useful for exercise-induced bronchospasm. It if effective only for the prophylaxis of asthma and is not used in an acute asthma attack.

Answer E: Theophylline likely caused bronchodilation by inhibiting phosphodiesterae thereby decreasing cAMP hydrolysis by increased cAMP levels. It use is limited because of its narrow therapeutic window. Toxicity may manifest as cardiac or neurologic symptoms.

Bottom Line: Acute asthma exacerbations are treated with supplemental oxygen, beta-2 agonists and muscarinic antagonists. Exams are moving toward adding more and more media clips in the form of pictures, video or audio. You need to be able to diagnose many conditions based on common physical exam signs. In addition to lung sounds, you should try and learn to recognize how to diagnose murmurs based on what they sound like.

Question 2: A 12 year old female presents to the ER in severe respiratory distress. She complains of persistent cough, dyspnea and chest tightness. Physical exam reveals a decreased inspiratory to expiratory duration, accessory muscle use, tachypnea, tachycardia, and decreased breath sounds. Upon further auscultation you hear the breath sound in the exhibit below. What is the most likely diagnosis?

Asthma

Inhaled foreign body

Lobar pneumonia

Interstitial pneumonia

Pleuritis

Explanation:

The most likely diagnosis is asthma. Asthma is a reversible airway obstruction secondary to bronchial hyperreactivity, airway inflammation, mucous plugging and smooth muscle hypertrophy. Patients often present with cough, episodic wheezing, dyspnea, and chest tightness. Symptoms often worsen at night or early in the morning. Physical exam reveals wheezing, prolonged expiratory duration (decreased inspiratory to expiratory ratio), accessory muscle use, tachypnea, tachycardia, decreased breath sounds (late sign), decreased oxygen saturation (late sign), hyperresonance and possible pulsus paradoxus. Arterial blood gases demonstrate mild hypoxia and respiratory alkalosis. Normalizing PCO2, respiratory acidosis and more severe hypoxia in an acute exacerbation warrant close observation as they may indicate fatigue and impending respiratory failure. Spirometry may show a decreased FEV1/FVC ratio. Eosinophilia may be seen on a CBC while a CXR shows signs of hyperinflation. Asthma can be definitively diagnosed with a methacholine challenge test. Treatment in general includes avoiding allergens and potential triggers, beta-2 agonists, corticosteroids, muscarinic antagonists, methylxanthines, cromolyn and antileukotrienes.

Answer B: An inhaled foreign body may present with stridor. Stridor is a high pitched wheezing that is caused by the obstruction of the trachea either by inflammation or an object. Just enough air passes the obstructed point to cause a high-pitched whining wheeze. An inhaled foreign body may become lodged in the trachea or mainstem bronchus. Radiographs may show signs of hyperinflation. Treatment consists of rigid bronchoscopy.

Answer C: Lobar pneumonia may present with rales, whispered pectoriloquy or egophony on physical exam. It can be acute in onset and caused by various organisms depending on certain patient demographics.

Answer D: Interstitial pneumonia may present with rales, whispered pectoriloquy or egophony on physical exam. It can be acute in onset and caused by various organisms depending on certain patient demographics.

Answer E: Pleuritis is inflammation of the pleural lining of the lung. It can present with pleuritic chest pain which is defined as a knife-like pain on inspiration and may be caused by a number of disorders such as a PE or infection. It often presents with a pleural friction rub on physical exam. Pleural Friction Rubs are created when the visceral and parietal pleurae become inflamed and roughened. The inflamed membranes will stick together. As the therapist auscultates the chest wall, the rubbing together of the inflamed membranes will cause the patient to experience pain and stop breathing - a maneuver called splinting. The pain is caused by the sticking together of the membranes and the pulling apart of those membranes with continued breathing. Once the membranes slip past one another and break free from the sticking point, then the patient is pain-free and inhalation or exhalation can continue. The sound that a pleural friction rub makes is a leather-on-leather type of sound. These sounds can be heard at the same points in the inhalatory and the exhalatory cycles.

Bottom Line: Wheezing is a common type of breath sound heard in patient with asthma. Exams are moving toward adding more and more media clips in the form of pictures, video or audio. You need to be able to diagnose many conditions based on common physical exam signs. In addition to lung sounds, you should try and learn to recognize how to diagnose murmurs based on what they sound like. For more information, see: http://www.uptodate.com/contents/asthma-symptoms-and-diagnosis-in-children-beyond-the-basics

Question 3: A mother brings her 10 year old son to the office for a follow-up examination to discuss pulmonary function test results that were preformed last week. You inform her that your suspicions have been confirmed and her son has asthma. She begins to tell you how she has looked up asthma on the internet and refuses to put her son on any steroids. You would then discuss the following medication as an option for long term control with the patient's mother:

Albuterol

Prednisone

Salmeterol

Theophylline

Montelukast

Explanation:Montelukast (Singulair) is a leukotriene receptor antagonist that may be used as an alternative to inhaled glucocorticoids as a long-term asthma control agent.

Answer A: Albuterol is a short-acting beta agonist and is used acute relief of asthma and is not recommended for chronic control of the illness

Answer B: Prednisone should not be started at this time because of the requests made by the patient’s mother. This would prohibit all steroids from being given at this time

Answer C: Salmeterol is a long-acting beta agonist, which can be used for the long term management of asthma. However, due to recent studies linking the long-term use of long-acting beta agonists to increased mortality, salmeterol should only be used in combination with inhaled glucocorticoids, and never as monotherapy.

Answer D: Theophylline is incorrect because is used mostly in hard-to-control asthmatics and has a high side effect profile.

Bottom Line:  Bottom Line: An alternative to steroid treatment for asthma includes leukotriene receptor antagonists such as montelukast. We cannot emphasize enough how important it is to have a clear understanding of the correct approach to managing an asthmatic patient. Asthma is an extremely high-yield topic. Remember that ABG analysis may show mild hypoxia and respiratory alkalosis. Look for decreased FEV1 on pulmonary function tests. Regarding medication protocols for the treatment of chronic asthma, disease severity can be divided into 3 basic categories: mild, moderate, and severe. Always remember to treat cases of statis asthmaticus (prolonged, non-respondable asthma attack) with aggressive bronchodilatory therapy, corticosteroids, O2, and intubation if necessary. Remember AIRWAY, AIRWAY, AIRWAY!!! Mild (infrequent exacerbations): Treat only with inhaled short-acting beta-agonists during an attack. Moderate (daily and/or occasional nighttime attacks): Treat with inhaled beta-agonist and inhaled corticosteroid with consideration of adjunct therapy with cromolyn or a leukotriene inhibitor. Severe (multiple daily and nighttime attacks): Treat with inhaled beta-agonist, inhaled corticosteroid, and multiple additional therapies including systemic steroids.

Question 4: A 16 year old female presents to your office with shortness of breath with light activity. After examination and testing, she is determined to have asthma. The pharmacologic therapy that is likely to have the biggest impact on her FEV1 is:

IV epinephrine

Inhaled corticosteroids

Inhaled beta-2 agonist

IV beta-2 agonist

SQ epinephrine

Strokes

Strokes and TIAs will 100% for sure be on your PANCE/PANRE/PACKRAT/EORs, you name it. While historically, the PANCE and PACKRAT are only 6% Neurology questions, these are a few that you shouldn’t miss. After completing my general neurology rotation, I quickly learned that the answers to these complex puzzles was definitely time-dependent. Can you think on your feet and generate a differential diagnosis? Attention to tiny details was crucial for Neurology because that’s how you can tell what part of the brain the ischemia/infarction is coming from.

I hope this review helps you regardless of which avenue you find it useful. Good luck and make sure to check out TrueLearn’s free sample questions below! The vignette style questions are exactly what you need to prepare yourself for EOR and PANCE related questions. Good luck!

Transient Ischemic Attack, Cerebrovascular Accidents (CVA) or Stroke, Bell’s Palsy

Evolving stroke: worsening

Completed stroke: maximal deficit has occurred

Duration of symptoms is the determining difference

Transient Ischemic Attacks (TIA)

Neurologic deficit that lasts few mins to <24 hours (N: 30 mins)

Symptoms transient because reperfusion occurs due to collateral circulation or breaking up of embolus

Blockage in blood flow does not last long enough to cause permanent infarction

Clinical Pearls

Triptans are contraindicated in patients with coronary artery disease or peripheral vascular disease and should be avoided in all patients with an increased risk for stroke

Contraindications to thrombolytic therapy: previous hemorrhagic stroke, stroke within 1 year, a known intracranial neoplasm, active internal bleeding, suspected aortic dissection. Relative contraindications: severe uncontrolled hypertension, use of anticoagulation, active peptic ulcer disease.

Hypertension is the most common and most important stroke risk factor

Ischemic Stroke (85%)

Causes in young patients: OCP use, hypercoagulable states (pregnancy, malignancy, vWF, antiphospholipid antibody syndrome), vasoconstrictive drug use (cocaine, amphetamines), polycythemia vera, sickle cell

RF: age and HTN, smoking, DM, hyperlipidemia, atrial fibrillation (cardioembolic), family history of CAD, family history of stroke, previous stroke/TIA, carotid bruits, drugs (sympathomimetics, OCPs, cocaine)

Clinical manifestations

See Table 1 Below

1. CT without contrast of head - differentiates ischemic from hemorrhagic (first line), may have to wait 24-48 h to see infarct

2. MRI of brain - more sensitive than CT and identifies ALL infarcts earlier than CT, not preferred in emergent setting

3. EKG - acute MI or A-fib may be cause of embolic strokes

4. Carotid duplex scan - determines degree of stenosis

5. MRA - definitive test for stenosis of vessels of head/neck and for aneurysms

Acute - supportive treatment (airway protection, O2, IV fluids)

1. C-A-B

2. Gradual BP Control - do not give antihypertensives UNLESS

SBP >200, DBP >120 or MAP >130 mmHg

Preferred: IV Labetalol 20 mg

Acute MI, aortic dissection, severe HF, hypertensive encephalopathy

Receiving thrombolytic therapy

Prevention

-Control RF: HTN, DM, smoking, cholesterol, obesity

-Aspirin

-Carotid endarterectomy

-Prevention of lacunar strokes: control HTN

Stable

1. t-PA therapy

A. If administered within first THREE hours of onset, improved outcome at 3 months

B. Do not initiate if: >3 hours, uncontrolled HTN, bleeding disorder or anticoagulated, history of recent trauma or surgery

C. Do not give aspirin for first 24 hours if t-PA given, perform frequent neuro checks, carefully monitor BP

2. Aspirin is best if given within 24 hours of symptom onset

A. If within 3 hours - give thrombolytics

B. If after 3 hours - give aspirin, and if pt allergic, give Clopidogrel → Ticlopidine

3. Anticoagulants (heparin/warfarin) have not been proven to have efficacy in acute stroke

4. Assess patient’s ability to protect airway, keep NPO, elevate HOB to 30 degrees

Embolic Stroke

Most common type

MC location: heart (due to embolization of mural thrombus in pt with atrial fibrillation), internal carotid, aorta, paradoxical

1. Onset of symptoms very RAPID (seconds), and deficits are maximal initially

2. Clinical features depend on artery occluded

3. MCA most commonly affected: A. Contralateral hemiparesis (weakness)

B. Hemi-Sensory loss

C. Hyperreflexia

D. Aphasia (90% left)

E. Apraxia

High risk of stroke in subsequent months

-Risk is 10% per year

-30% 5-year risk of stroke

Thrombotic Stroke

Atherosclerotic lesions in large arteries of neck or medium sized arteries of brain (MCA)

1. Onset may be rapid or stepwise

2. Patient awakens from sleep with neurologic deficits

Lacunar Stroke (internal capsule, pons, thalamus)

Causes 20% of all strokes; usually affects subcortical structures

Narrowing of large arterial lumen due to thickening of vessel wall (not by thrombosis)

RF: history of chronic HTN and DM

Affected arteries: MCA, Circle of Willis, basilar and vertebral arteries

Hemiparesis - weakness of entire left or right side

1. Internal capsule: Pure motor hemiparesis

2. Pons: Dysarthria, clumsy hand

3. Thalamus: Pure sensory deficit

Focal features and usually contralateral pure MOTOR or pure SENSORY deficits

-Prevention of lacunar strokes: control HTN

Transient Ischemic Attack

Brief episode of neurologic dysfunction caused by focal brain or retinal ischemia

Blockage in flow does not last long enough to cause permanent infarction

Retinal artery (MCA) → amaurosis fugax

1. Sudden onset neurologic deficit

2. Lasts minutes to <1 hour (N: 15-30 minutes)

2. Reversal of symptoms within 24 hours

1. Carotid doppler ultrasound  

2. MRA of neck

1. Hospital admission for new onset and recurrent TIA, unless confident diagnosis of cause of event can be made

2. Antiplatelet therapy: Aspirin +/- dipyridamole OR Clopidogrel

NOTE: If high risk → Warfarin should be used

RF for recurrent stroke, average 5% risk per year

Amaurosis Fugax

Etiology: atherosclerosis (emboli to the ophthalmic artery), carotid stenosis

“Fleeting blindness” or “curtain coming down” vertically into field of vision

1. Painless, transient

2. Unilateral (monocular) vision loss

3. Seconds of a graying out of vision in one eye

Retinoscopy: refractile arterial lesions (Hollenhorst plaques, cholesterol crystals)

Annual risk of stroke is 1-2%

Carotid Stenosis

Extracranial internal carotid artery stenosis >80% +/- symptoms of ischemia

Asymptomatic - refers to presence of narrowing of the ICA in individuals without a history of recent ipsilateral ischemic stroke or TIA

Symptomatic - refers to neurologic symptoms caused by TIA or ischemic stroke in the carotid artery territory and ipsilateral to significant carotid atherosclerotic pathology

Symptoms of ischemia

1. Partial and complete blindness in one eye and absent pupillary light response

2. Contralateral homonymous hemianopsia, hemiparesis, hemisensory loss

3. Left hemisphere - Aphasia

4. Right hemisphere - left visuospatial neglect, constructional apraxia, dysprosody

5. Unilateral limb shaking, transient loss of monocular vision upon exposure to bright light

6. Does NOT cause vertigo, lightheadedness, or syncope

Signs

1. Carotid bruit

2. Funduscopic exam: arterial occlusion or ischemic damage to retina

1. Cerebral angiography (gold standard)

-Permits use of entire carotid system, provides info about tandem atherosclerotic disease, plaque morphology, and collateral circulation

-Identifies people who would benefit from endarterectomy (CEA)

2. Carotid duplex ultrasound

-Non-invasive, but hairline residual lumens can be missed and can overestimate degree of stenosis

3. Magnetic resonance angiography (MRA) neck

-Less accurate for detecting moderate stenosis, more expensive, time consuming, patient must lie still, renal insufficiency can be an issue

4. CT angiography (CTA)

-Impaired renal function is a relative contraindication since contrast bolus must be given (DM/CHF)

See treatment of asymptomatic and symptomatic CAS below

Asymptomatic Bruits

1.Start daily antiplatelet therapy, statin therapy, manage diabetes, treat hypertension, and healthy lifestyle (limit ETOH consumption, weight control, aerobic physical activity, Mediterranean diet)

2. Carotid endarterectomy (CEA): >80% stenosis, recurrent TIAs on medical therapy (preferred)

-If patient has life expectancy of >5 years

3. Duplex ultrasonography - repeat annually to assess progression or regression of disease and response to therapeutic intervention if stenosis >50%

4. Carotid artery stenting (CAS) only for high risk patients

-Unlikely to benefit if: severe comorbidity, prior ipsilateral stroke, total occlusion of ICA

Symptomatic Bruits - manifested as recent TIA or ischemic stroke and ipsilateral CAS

1. Anticoagulation (Warfarin)

2. Carotid endarterectomy (CEA) indicated for  

-Severe stenosis (70-99%) → CEA recommended

-Mod stenosis (50-69%) → CEA recommended

-Mild stenosis (<50%) → no indication for CEA or carotid angioplasty with stenting

-Consider AGE: If >70, CEA may be associated with better outcome compared to CAS; for younger patients, CAS = CEA in terms of periprocedural complications

3. CAS is indicated as an alternative to CEA for symptomatic patients at average or low risk of complications when diameter of lumen of ICA is reduced by >70% by non-invasive imaging, or >50% by catheter angiography, or >50% by noninvasive imaging with corroboration

High risk: progression of asymptomatic CAS, detection of embolism, plaque burden and morphology, reduced cerebrovascular reserve, silent embolic infarcts

Bell’s Palsy: hemifacial weakness/paralysis of muscles innervated by CN 7 due to swelling of cranial nerve

Uncertain cause, possibly viral (herpes simplex)

1. URI preceding event

2. Acute onset unilateral facial weakness/paralysis, both UPPER and LOWER parts of face affected

3. Weak orbicularis oculis muscle (cannot raise eyebrows) on affected side

Clinical diagnosis

--Consider Lyme disease (do not use steroids)

--EMG testing if paresis fails to resolve in 10 days

--Usually no treatment required

--Short course of prednisone and acyclovir

--Wear eye patch to prevent corneal abrasion

--Surgical decompression of CN 7

Prognosis good: 80% recover fully within weeks to months

Table 1. Deficits Seen in Ischemic Strokes

Distribution

Location and/or Type of Deficiency

Anterior Cerebral Artery (ACA)

1. Contralateral lower extremity hemiparesis and hemisensory loss (leg > arm)

2. Abulia (especially if bilateral) - inability to make decisions

Middle Cerebral Artery (MCA)

1. Aphasia (if dominant hemisphere involved) - 90% LEFT

2. Agnosia (non-dominant) - inability to process sensory information

2. Apraxia, contralateral body neglect, confusion (if non-dominant hemisphere involved)

3. Contralateral hemiparesis and hemisensory loss

4. Homonymous hemianopsia (variable)

Internal Carotid Artery (ICA)

1. Ipsilateral blindness (variable)

2. MCA syndrome

Vertebral or PICA (posterior inferior cerebellar artery)

1. Ipsilateral: hemiataxia, nystagmus facial sensory loss, Horner syndrome  

2. Contralateral loss of temperature or painful sensation

3. Dysphagia

Basilar Artery

1. Quadriparesis

2. Dysarthria

3. Dysphagia

4. Diplopia

5. Somnolence

6. Amnesia

Posterior Cerebral Artery

1. Contralateral homonymous hemianopsia

2. Amnesia

3. Sensory loss

Lacunar (internal capsule, pons, thalamus)

1. Internal capsule: Pure motor hemiparesis

2. Pons: Dysarthria, clumsy hand

3. Thalamus: Pure sensory deficit

Unfortunately, cocaine use is one of the main causes of stroke in the young

Common sites of SAH

Junction of anterior communicating artery & anterior cerebral artery

Junction of posterior communicating artery & internal carotid

Bifurcation of the MCA

CHADS2 Scoring

The presence of congestive cardiac failure (C), hypertension (H), age >75 years (A), and diabetes (D) each scores one point, and a history of prior stroke or TIA (S) scores two points. A CHADS score of two or more is associated with an annual risk of stroke of over 4%.

International treatment recommendations are aspirin 325 mg/day for those with a CHADS score of 0

For those with a CHADS score of 1, aspirin or warfarin may be used depending on patient preference.

Patients with a CHADS score of 2 or more should be anticoagulated unless there is a specific contraindication.

Patients with bacterial endocarditis should not receive warfarin because of the risk of cerebral hemorrhage from septic embolization.

Subarachnoid Hemorrhage or Cerebral Aneurysm, Intracerebral Hemorrhage (ICH)

Hemorrhagic Stroke (15%)

Intracerebral Hemorrhage (ICH): bleeding into the brain parenchyma

NOTE: In the acute phase, the mass effect of a cerebral hematoma is far greater than in a large cerebral infarction with a greater risk of herniation and death

In chronic phase, prognosis is much better for those with hemorrhage than those with ischemia

Causes: HTN (sudden increase) is most common cause

-Ischemic stroke convert to → hemorrhagic stroke

Patient develops edema around lesion or expansion of hematoma → herniation of brain tissue

Locations: putamen (40%), thalamus, lobar white matter, caudate, pons, cerebellum

RF: smoking, advanced age, anticoagulant use

1. Abrupt onset of a focal neurologic deficit worse steadily over 30-90 minutes

-Pinpoint pupils - pons

-Poorly reactive pupils - thalamus

-Dilated pupils - putamen

-Decreased level of consciousness

2. Headache, nausea, vomiting

- Severity of headache correlates with size of lesion

3. Confusion, aphasia, hypersomnolence

Signs

1. Increased ICP

2. Intubated

3. Hypertensive

4. Hyperconvergence, absent vertical gaze, horizontal gaze paresis

5. Sensorimotor: hemiparesis, hemisensory or hemimotor loss, quadriplegia, ataxia

6. Stupor, coma

1. Non-contrast CT scan of head (90% of ICH): hyperintense area with mass effect and (later) hyperintense surrounding edema

2. CT Angiography

-Coag panel and platelets

-Ophthalmologic examination is mandatory to rule out papilledema

1. Admit, supportive care, control BP

a. IV Labetalol, Esmolol, or Nicardipine (Cardene)

-Target: SBP <180

-MAP <130

B. Reverse anticoagulants: FFP + Vitamin K, Protamine

-Mannitol (osmotic agent) and diuretics to reduce ICP

-Steroids harmful, NOT recommended

-Rapid surgical evacuation of CEREBELLAR hematomas only

2. Emergent neurosurgery consult

High mortality rate (50% at 30 days)

3. Surgery if >3 cm

STEROIDS CONTRAINDICATED

Complications: increased ICP, seizures, rebleeding, vasospasm, hydrocephalus, SIADH

Cerebral (intracranial) Aneurysm

--Develops from normal hemodynamic stress or HTN

--Develops at junction of communicating branch with main cerebral artery (Ant Comm + Ant Cerebral)

AV malformation

Causes:

1. Ruptured berry (saccular) aneurysm (MCC, 80%) - most located in anterior circulation

2. Fusiform (large)

3. Mycotic (bacterial endocarditis)

Associated: polycystic kidney disease, Marfan syndrome

May manifest as compression as cranial nerves (CN 3, 4, 6)

Causes of rupture: strenuous activity (exercise, coitus, physical work)

1. Non-contrast CT head - if normal, do LP

a. Contrast CT or MRI for aneurysms >5 mm or AV malformations

2. Lumbar puncture

3. Cerebral angiography (gold standard)

1. Open surgical clipping

2. Endovascular coiling (preferred)

Complication: Subarachnoid Hemorrhage

Of aneurysms that rupture, 33% die before reaching the hospital, 20% die in the hospital, 30% recover without disability

Subarachnoid Hemorrhage (SAH): bleeding into the CSF; outside brain parenchyma

RF: smoking, hypertension, cocaine and alcohol use, first-degree relative with SAH, female, African-American, connective tissue disorders

“Thunderclap headache”

Locations: saccular aneurysms at bifurcations of arteries of the Circle of Willis

1. Sudden onset severe headache (excruciating)

-Absence of focal neurologic deficit

-”Worst headache of my life”

-Sudden, transient loss of consciousness

2. Nausea, vomiting (common)

3. Neck pain, nuchal rigidity

4. Photophobia, visual changes

5. Decreased level of consciousness (53%)

6. Seizure (20%)

Signs

1. Hypertensive

2. Retinal hemorrhage (30%)

1. Fundoscopic exam: retinal hemorrhage

2. Non-contrast CT (first line): negative in 10%

→ if negative, follow with CSF

-Most are negative <2 hours, most sensitive >12 hours

3. Lumbar Puncture

-CI: elevated ICP, thrombocytopenia, suspected epidural abscess

-Xanthochromia, elevated RBCs

1. Blood in CSF (Hallmark)

2. Xanthochromia (yellow CSF) is gold standard for diagnosis, resulting from RBC lysis by 6 hours

4. CT Angiography

5. Once diagnosed → cerebral angiogram (definitive)

1. Supportive care, admit

A. Bed rest in quiet, dark room

B. Stool softeners to avoid straining

C. Analgesia for headache (tylenol)

D. IV fluids for hydration

E. Lower BP gradually using CCB (Nifedipine) for vasospasm

2. Craniotomy and clipping - definitive

-Coiling: alternative

3. Treat BP aggressively

-PO Nimodipine 60 mg should be given x 21 days after to prevent vasospasm

High mortality (40-50% at 30 days)

Most rebleeding occurs within first 3 days after rupture

Complications: rerupture (30%), vasospasm (50%), hydrocephalus, SIADH, hypertension

TrueLearn Questions

Question 1: A 60-year-old woman with a presents to the emergency department because she suddenly “felt her left arm go heavy and numb.” Approximately half an hour prior to arrival at the hospital, she noticed that she could no longer lift her spoon to her mouth. She has not had surgery, head trauma, stroke, or gastrointestinal or urinary bleeding recently. Medications include lisinopril, atorvastatin, metformin, glyburide, nifedipine, aspirin, and clopidogrel. On examination, her temperature is 37ºC (98.6ºF), heart rate is 89 beats/minute, respirations are 18 breaths/minute, and blood pressure is 175/100 mmHg. There is asymmetry of the nasolabial folds and mouth. Pupils are equally round and reactive. There is 2/5 strength in the left upper extremity and 5/5 strength elsewhere. Light touch, pinprick, vibration, and proprioception are markedly diminished in the left upper extremity and intact elsewhere. Head CT shows no evidence of intracranial hemorrhage. Which of the following is true of the use of fibrinolytic therapy in the treatment of this patient?

Blood pressure must be reduced to less than 170/100 mm Hg before starting fibrinolytic therapy

Fibrinolytic therapy can be given up to 4.5 hours after symptom onset

Fibrinolytic therapy is contraindicated because the patient is taking clopidogrel

Fibrinolytic therapy is contraindicated in chronic renal failure

Fibrinolytic therapy is contraindicated in the setting of recent transient ischemic attack

Explanation:

This patient most likely has suffered an ischemic stroke given her neurologic symptoms. Head CT is negative for intracranial bleed, and her symptoms began 30 minutes prior to arrival to the hospital; therefore, she is a good candidate for thrombolytic therapy. Fibrinolytic therapy can be given up to 4.5 hours after symptom onset or after the patient was last known to be normal, if the time of onset of symptoms is not known. After 4.5 hours mortality associated with fibrinolysis exceeds that associated with stroke. Contraindications to fibrinolytic therapy include: history of intracranial hemorrhage, blood pressure > 185/110 mm Hg, myocardial infarction within three months, major surgery within 14 days, stroke or head trauma within 3 months, INR > 1.7, platelets < 100,000, clearing symptoms, and seizure such that symptoms may be post-ictal rather than due to stroke. If the patient presents within the first 3 hours following onset of symptoms, he/she will receive tissue plasminogen activator (tPA). Between 3 and 4.5 hours, patients can receive recombinant tPA. Additional contraindications to this treatment include age greater than 80, anticoagulation regardless of INR, and history of diabetes.

Answer A: Blood pressure reduction is not a necessary step in preparation for fibrinolytic therapy. This woman's blood pressure is already below the 185/110 mm Hg required for therapy.

Answer C: Use of clopidogrel or other anti-platelet medications is not a contraindication to fibrinolytic therapy; however, use of anticoagulants such as heparin or warfarin is a contraindication.

Answer D: Fibrinolytic therapy is not contraindicated in patients with chronic renal failure.

Answer E: Recent transient ischemic attack (TIA) is not a contraindication to using fibrinolytic therapy. A history of stroke within the last three months, however, is an absolute contraindication.

Bottom Line: Fibrinolytic therapy can be given up to 4.5 hours after symptom onset or after the patient was last known to be normal, if the time of onset of symptoms is not known. For more information, see http://emedicine.medscape.com/article/1160840-overview

Question 2: A 76-year-old male presents to the emergency department with a chief complaint of an inability to move his right upper and lower extremity after waking from a nap an hour ago. A mild aphasia and contralateral facial droop are noted on physical exam. A CT scan (without contrast) of the head reveals dark areas within the middle cerebral artery distribution. During physical examination the patient develops a sudden headache, right pin-point pupil and poor gag reflex with increased respiratory effort. The most appropriate course of action is

Administer thrombolytic therapy (t-PA)

Immediate intubation

Immediate neurosurgical consultation

Rapid nitroprusside infusion to reduce blood pressure

Repeat stat CT scan without contrast

Explanation:

In the case above the patient presented with an ischemic stroke that converted to a hemorrhagic stroke. In a classic presentation of a thrombotic stroke a patient awakens from sleep with neurologic deficits. Though hypertension is the most common cause of a hemorrhagic stroke, an ischemic stroke may convert to a hemorrhagic stroke. A hemorrhagic stroke presents with headache, vomiting, altered level of consciousness and signs of increased intracranial pressure (ICP). In a patient that displays an altered mental status and respiratory drive, CABs with airway management takes precedence and intubation is frequently required. A head CT scan without contrast is ordered as the first imaging study to differentiate an ischemic from a hemorrhagic stroke. Ischemic strokes appear as dark areas on the CT scan while hemorrhagic strokes appear white.

Answer A: Thrombolytic therapy should not be administered in a patient with a suspected intracranial bleed. t-PA is administered for an acute ischemic stroke within three hours of symptom-onset.

Answer C: Though surgery for hematoma evacuation may be required later, the moreimmediate treatment is airway management

Answer D: Elevated blood pressure increases ICP and can cause further bleeding. BP reduction must be gradual (not rapid) to prevent hypotension which can lower cerebral blood flow and worsen neurological deficits.

Answer E: A repeat CT scan is necessary for the new neurological change. However, more immediate treatment is airway management.

Bottom Line: An ischemic stroke may convert to a hemorrhagic stroke. Any patient with a mental status change and an altered respiratory drive with poor gag reflex requires evaluation of CABs with appropriate airway management. insight: If a patient's airway is compromised, always start with CAB’s first, no matter what the clinical scenario may be.

Question 3: A 61-year-old man with no significant medical history presents to the emergency department after experiencing difficulty speaking at a work holiday party two hours ago. He says that he was talking to a co-worker and suddenly could not find the words to finish the story he was telling. He sat down for a few minutes but finally decided to seek care when he realized that his right hand was weak and his speech had not returned. His symptoms started to resolve shortly before arriving at the emergency department and he says he feels better now but he thinks he is “not quite himself.” His only medicine is a daily multivitamin. On exam he is afebrile, and all vital signs are within normal limits. His speech is somewhat slow and his face is slightly asymmetric. Grip strength in his right hand is 4+/5. No other neurological abnormalities are noted. His cardiac exam shows a regular rate and rhythm with no murmurs, rubs, or gallops. His lungs are clear to auscultation. CT scan shows no abnormalities, and the patient refuses MRI due to claustrophobia. Which of the following is the next best step in the management of this patient?

ECG

Factor V Leiden screen

Lumbar puncture

Syphilis serology

Transthoracic echocardiography

Explanation:

This patient is exhibiting signs of a transient ischemic attack (TIA). All the tests listed are reasonable in the workup of TIA but evaluation for cardiac arrhythmias as a possible embolic source is the most urgent of the listed options. Bottom Line: TIA needs to be investigated for a cause in order to prevent ischemic stroke in the future. Most patients will require a full cardiac workup in addition to brain imaging.

Question 4: A 45 year-old female with a history of hypertension presents to the emergency department complaining of the worst headache of her life. A CT scan is performed and found to be negative. A lumbar puncture demonstrates xanthochromia. What is the most likely vessel(s) associated with her condition?

Posterior cerebral artery and basilar artery junction

Posterior cerebral artery and posterior communicating artery junction

Anterior communicating artery and anterior cerebral artery junction

Middle cerebral artery and internal carotid artery junction

Middle meningeal artery

Explanation:

Intro to Electrocardiograms for Physician Assistants

Updated: 07/08/2016

Electrocardiocardiograms can be difficult to tackle and I know that this is a topic that I repeatedly visit, both for simple things like delineating PVCs (premature ventricular contractions) from PACs (premature atrial contractions) and denoting what defines a second degree type 1 versus a second degree type 2 heart block. But there’s so much more than just that - there’s right and left bundle branch blocks, right and left ventricular hypertrophy, ischemia, infarction, axis deviation, atrial hypertrophy, etc. While this is a very limited approach to EKGs and while there is still much to learn about them, this is a great introduction to EKGs for any student, whether you are pre-med, pre-PA, pre-NP, pre-nursing, or pre any other health profession. At the end of the review are a few helpful questions provided by TrueLearn you can use after you’ve studied the review, which offer you some insight into the type of questions and degree of exam preparation offered. I hope that you find them as useful as I have. Good luck and let me know if there are any errors or questions!

Electrocardiogram (ECG): records the electrical activity of the heart and information about the heart’s function and structure

Basic Principles

A polarized myocyte has a negatively charged interior and positively charged outside surface = resting state

Depolarization - occurs when myocytes interiors become positive and contraction occurs

Repolarization - recovery phase occurring immediately after depolarization

When a wave of positive Na+ ions moves toward a positive electrode, an upward deflection is recorded

The SA Node (upper posterior wall of right atrium) initiates depolarization at regular intervals stimulating both atria to contract and producing a P-wave (atrial depolarization)

The tricuspid and mitral (AV) valves lie between atria and ventricles, providing electrical insulation, leaving only the AV node to conduct depolarization

tRIcuspid on the RIght side

AV valves also prevent backflow into the atria

The AV Node - slow conduction by calcium ions

Represents brief pause after P-wave before QRS complex

Ventricular Conduction System

QRS Wave (Purkinje Fibers): His Bundle → Left and Right Bundle Branches

Ventricular depolarization is rapidly conducting Na+ ions, represented by the QRS complex

Q wave: first downward deflection of the QRS complex

R wave: first upward wave of QRS complex

S wave: any downward wave preceded by an upward wave

ST segment: horizontal baseline following QRS wave

T-wave: represents the rapid phase of ventricular repolarization

Repolarization is accomplished by potassium (K+) ions leaving monocytes

Ventricular systole (contraction) begins with the QRS complex and lasts until the end of T wave

QT Interval: duration of ventricular systole; measured from beginning of QRS until end of T wave → good indicator for repolarization

Long QT Syndromes are vulnerable to dangerous (deadly) rapid ventricular rhythms

QTc: Precise QT interval measurements are corrected for rate

Calculated by dividing the measured QT by the square root of the R-R interval

QTc >0.46 seconds = LQTS

Considered normal when less than half of the R-to-R interval

PR Interval: P wave + PR segment

U-wave (follows T wave): repolarization of the Purkinje fibers

Physiology

Sympathetic Nerves

Secrete Norepinephrine that activates adrenergic receptors

The heart is stimulated by the sympathetic NS that deliver NE to the B1 adrenergic receptors, producing an excitatory response

Cardiac excitatory effects: increased rate of SA Node pacing, rate of conduction, contractility, and irritability of foci

Epinephrine is secreted by the adrenal glands and is more potent than NE in stimulating B1 receptors

Stimulation of arterial A1 adrenergic receptors constricts arteries throughout the body increasing blood pressure and flow (more responsive to NE)

Parasympathetic Nerves

Secrete Acetylcholine (ACh) that activates cholinergic receptors

Cardiac inhibitory effects: decreased rate of SA node pacing, rate of conduction, contractility, irritability of atrial and junctional foci  

Arterial cholinergic receptors respond by dilating arteries and reduce blood pressure and flow

The cardiac cycle represents atrial systole (contraction), followed by ventricular systole (contraction) and resting stage that follows until another cycle begins

Atrial depolarization represented by the P wave

Actually lasts longer than the P wave

QRS complex represents ventricular depolarization

Actually lasts longer than the QRS complex

The release of free calcium ions into the interior of the myocytes produces contraction

Repolarization is due to controlled outflow of K+ ions from myocytes

Cell to cell conduction through the myocardium is carried by Na+ ions, however, AV nodal conduction is due to slow movement of calcium ions

ECG Recordings

Small boxes are 1 mm by 1 mm; each small box represents 0.04 seconds and large boxes of 5 small boxes represents 0.2 seconds

Heavy black lines are separated by 5 small squares

Time axis is horizontal and the vertical axis represents voltage

Upward deflections are positive, downward deflections are negative

The Standard 12-Lead ECG

Electrodes are placed on the R arm, L arm, and L leg

Einthoven’s Triangle

Leads I, II, and II: Each bipolar limb lead is recorded using 2 electrodes, one being positive and the other negative

RAN = right arm negative, LLP = left leg positive, and you can always figure out the left arm from there

Unipolar Limb Leads: AVF signifies the left leg electrode, which is termed AVF (Augmented Voltage, left Foot) by Dr. Goldberger who discovered that we must amplify the voltage in the machine to match the magnitude of each of the leads

AVR (right arm), AVL (left arm), AVF (left foot) - all positive

All six limb leads form an intersection that lie in a flat frontal plane of the patient’s chest

The importance of the positive electrode’s position is emphasized by the conventional grouping of limb leads

The ‘lateral leads’ refers to lead I and AVL (positive left arm electrode), which is important for recognizing lateral wall ischemia/infarction

The ‘inferior leads’ refers to leads II, III, and AVF (positive left foot electrode), which is important for recognizing inferior wall ischemia/infarction

The chest leads (V1-V6) are oriented through the AV node and projections anterior to posteriorly through the patient’s back, which is negative

The plane is called the horizontal plane

V1 and V2 cover the right ventricle, signify the anterior wall

V5 and V6 cover the left ventricle and signify the lateral wall

Leads V1-V6 should gradually change

V1’s QRS complex is normally more negative  

V6’s QRS complex is normally more positive

V3 and V4 are oriented over the interventricular septum (right and left bundle branches course through)

V5 and V6 are called the left chest leads and are positive because of their position around the heart; greater upward deflections are caused by depolarization moving toward the positive electrode

Terminology

Automaticity: the generation of pacemaking stimuli

Automaticity (ectopic) foci: focal areas of automaticity in the heart that are potential pacemakers capable of pacing in emergency situations; normally electrically ‘silent’

These have the ability to pace at their inherent rate if SA node ceases to function

Atria: 60-80/minute

AV Junction: 40-60/minute

Ventricles: 20-40/minute

SA node overdrive-suppresses slower pacemaker foci below it

All automaticity foci pace with a regular rhythm

Vagal Maneuvers: induced gagging or carotid sinus massage provide afferent input for parasympathetic reflexes that counterbalance sympathetic effects → can inhibit an irritable atrial or AV junctional focus or inhibit AV node completely increasing refractoriness

Arrhythmia (Dysrhythmia): without rhythm; denotes any abnormal rhythm

Absolute Refractory Period: no impulse possible

Relative Refractory Period: Impulse possible if stimulus strong enough

Parasystolic focus: an automaticity focus that has entrance block meaning the focus paces, but cannot be overdrive-suppressed; incoming depolarization is blocked, ‘protecting’ foci from passive depolarization by other sources (not healthy)

P’ (P prime): represents atrial depolarization by an automaticity focus, as opposed to normal sinus-paced P waves

Asystole: all activity ceases (straight line), no electrical activity

Pulseless electrical activity (PEA): rhythm on the monitor but no pulse

Unifocal: single ventricular focus in which all ectopic beats appear identical

Multifocal: several ventricular foci that have multiple configurations

Runs: 3+ premature ventricular contractions occurring in succession

Couplets: 2 PVCs attach to one another

Bigeminy: PVCs falling in a pattern of ‘every other beat’

Trigeminy: repetitive PVC followed by 2 sinus beats (3 beats)

Quadrigeminy: pattern of 4 beats (1 PVC and 3 sinus beats)

Heart blocks: caused when a supraventricular impulse is unable to be conducted normally through the ventricles because of a conduction disturbance at or below the AV node

Bundle Branch Blocks: caused by a conduction defect below the area of the node, within the branches of the ventricular conduction system

Non conducted P waves: “blocked” p waves or “dropped” QRS complexes

Agonal: dying heart, describes a terminal or lethal arrhythmia

Escape beat: comes later than expected and is a fail-safe to protect the heart

Method to Interpreting an ECG

Rate: number of cycles per minute

Sinus rhythm determined by SA node (pacemaker), normally 60-100

Sinus bradycardia: sinus rhythm <60/minute

Sinus tachycardia: sinus rhythm >100/minute

Determining the rate

The ‘300’ Method: Find an R wave that peaks on a heavy black line (start)

Works for regular intervals

Count off 300, 150, 100, 75, 60, 50 at each subsequent line (memorize this)

So a normal rate = R-R should be between 3-5 lines from one another

For bradycardias and irregular rhythms: Use The ‘3 Second’ Intervals Method

Identify the ‘3 second’ marks

Take 2 of the 3-second intervals and count the number of R-R wave cycles per 6 seconds

Multiply by 10 to get the number per minute

Rhythm

SA Node automaticity maintains a constant cycle duration between impulses, maintaining a regular rhythm

Irregularity: pauses, presence of too-early (premature) beats, sudden dramatic rate changes

Sinus Rhythms

Sinus Bradycardia

Rate: Slow <60

Rhythm: Regular

P-wave: normal

PR interval: Normal (0.12-0.20 s)

QRS: Normal (0.06-0.10 s)

Sinus Arrhythmia

Normal, but minimal, increase in heart rate during inspiration and extremely minimal decrease during expiration

Rate: Normal (60-100) and may increase with inspiration and decrease with expiration

Rhythm: Irregular (R-R varies without pattern)

P-wave: Uniform, one P wave for every QRS complex

PR interval: Normal (0.12-0.20 s)

QRS: Normal (0.06-0.10 s)

Sinus Tachycardia

Ex. hypotension, hypoxia, CHF, cardiomyopathy, myocarditis, anemia, fever, bleeding

Rate: Fast (>100)

Rhythm: Regular

P-wave: normal, may merge with T wave at very fast rates

PR interval: Normal (0.12-0.20 s)

QRS: Normal (0.06-0.10 s)

QT interval shortens with increasing rate

Irregular Rhythms

Wandering Pacemaker

Rate: Normal

Rhythm: May be irregular

P-wave: changing shape and size from beat to beat (>3 forms)

PR interval: variable

QRS: Normal (0.06-0.10 s)

T wave normal, if heart rate >100, rhythm may be MAT

Multifocal Atrial Tachycardia (MAT)

Ex. COPD, emphysema, digitalis toxicity

Rate: Fast >100

Rhythm: irregular

P-wave: changing shape and size from beat to beat (>3 forms)

PR interval: variable

QRS: normal (0.06-0.10 s)

Premature Atrial Complex (PAC)

Ex. Stress, hypoxia, stimulants (caffeine, tobacco, alcohol), valvular heart disease, CAD

Rate: Normal

Rhythm: irregular

P-wave: premature, positive, shape is abnormal; flattened, notched, peaked or diphasic; falls close to preceding QRS

PR interval: variable

QRS: 0.10 s or less (narrow)

Asymptomatic or palpitations

Observation

Beta blockers if SX

Junctional Tachycardia

Originates in the Bundle of His, 3 or more PJC’s in a row

Rate:

Atrial rate: 100-180

Rhythm: Regular

P-wave: superimposed on T waves  

PR interval: none

QRS: Narrow (<0.10 s)  

Atrial Tachycardia

Ex. Stress, hypoxia, stimulants (caffeine, tobacco, alcohol), COPD, valvular heart disease or CAD, ASD, or AMI

Arises from a focus in the atria

Presents as palpitations, light-headedness, and/or syncope

Rate: 150-250, atrial = ventricular

Rhythm: regular

P-wave: premature, positive, shape is abnormal (but present in front of each QRS)

PR interval: variable (0.12-0.20 s)

QRS: Normal

Transient, usually requires no treatment

Paroxysmal Supraventricular Tachycardia, PSVT

Originates above the ventricles

A descriptive term for indistinguishable Junctional tachycardia, atrial tachycardia, atrial flutter, and sinus tachycardia

Atrial rate: 150-250, may conduct to ventricles 1:1, 2:1, 3:1, or 4:1 in presence of block

Ventricular rate: 150-250

Rhythm: irregular

P-wave: premature, positive, shape is abnormal; may be absent  

PR interval: variable (<0.12 s)

QRS: Normal (<0.12 s)

Complication of Wolff-Parkinson-White Syndrome

Stable -

a. Vagal Maneuvers: Valsalva maneuver, bearing down, cough, breath holding, carotid sinus massage

b. Med - Adenosine IV 6 mg push, flush, 12 mg in 2 minutes (slows AV conduction and interrupts reentrant pathways)

Prevention -

a. Digoxin

b. Radiofrequency catheter ablation

Atrial Flutter

MCC: heart failure

Also, COPD, rheumatic fever, or ASD

AV node cannot conduct all impulses

Presents as palpitations, SOB, near syncope or syncope, CVA/TIA

Rate: Fast (250-350 atrial), slower ventricular rate (150-250)

Rhythm: Regular or irregular

P-wave: Non observable, saw-toothed flutter waves

PR interval: unmeasured

QRS: Normal (0.06-0.10)

Stable -

a. Rate control: BB or CCB Esmolol, Verapamil, Diltiazem

b. Cardioversion 50 J

C. Anticoagulants and rate control prior

Atrial Fibrillation (irregularly irregular)

Continuous chaotic atrial spikes from multiple irritable atrial foci, suffering from entrance block, pacing rapidly

At high risk for VTE and hemodynamic compromise if underlying heart disease

Most common causes: hyperthyroidism and mitral stenosis

Rate: Fast (>350 atrial, chaotic), slower ventricular rate

Rhythm: irregularly irregular

P-wave: No discernable p-waves

PR interval: unmeasured

QRS: <0.12 s (narrow)

Presents with fatigue, exertional dyspnea

1.If Stable -

a. Rate control: 60-100, Beta blockers preferred

-Non dihydropyridine CCB

b. Cardioversion to sinus rhythm (first A-fib, worsening, or hemo-unstable)

c. Anticoagulation to prevent CVA

-If present >48 h, anticoag with Warfarin for 3 weeks before and 4 weeks after cardioversion, INR 2-3

-May obtain TEE → IV heparin and cardioversion within 24 h

2. Unstable (decompensated HF, hypotension, uncontrolled angina): Cardioversion 200 J

3. Chronic A-Fib

-Rate control: BB

-Anticoagulation: not for young (<60)

4. New Onset - rate control

-CCB or BB: Diltiazem or Metoprolol

-Anticoag: IV Hep or LMWH

Ventricular Rhythms

Premature Ventricular Complex (PVC)

Single ectopic beat originating in the ventricles

Benign

Occur with ischemia or electrolyte disturbances

Occurs in patients with or without structural heart disease: hypoxia, electrolyte imbalance, stimulants, caffeine, meds, heart disease

Wide, bizarre QRS complexes followed by compensatory pause → p wave unseen because “buried” within QRS complex

Rate: Depends on underlying rhythm and number of ectopics

Rhythm: Regular

P wave: None, buried within QRS, compensatory pause

PR interval:

QRS: >0.12 (wide)

Asymptomatic or palpitations

If low CO → syncope, dizziness, sudden death

1. Observation!

2. BB or CCB if symptomatic, otherwise untreated

Patients with FREQUENT, REPETITIVE PVCs and underlying cardiac disease - increased risk for sudden death due with V. Fib  → electrophysiologic study

Ventricular Tachycardia: originates below bundle of His

“Wide QRS tachycardia”

HX of MI (Scar), ischemic CAD, QT prolongation, hypoxia, electrolyte imbalance, drug toxicity, CM

V-tach: 3+ consecutive ventricular premature beats

Rate: 100-250 bpm

Rhythm: Regular or irregular

P wave: none preceding QRS

PR interval: none

QRS: >0.12 (wide), bizarre but uniform

Sustained: persists in absence of intervention, lasts longer than 30 seconds, almost always symptomatic

-Hypotension, life-threatening → V-fib

SX: palpitations, dyspnea, lightheadedness, angina, syncope or near-syncope

-Sudden cardiac death

-Cardiogenic shock

-”Cannon A” waves in neck and S1 varying in intensity

Does not respond to vagal maneuvers or adenosine

1. Treat reversible causes

Sustained VT -

ACLS, shock, antiarrhythmics, CPR

a. Stable = IV amiodarone

b. Unstable = synchronous DC Cardioversion → IV amiodarone or Lidocaine

c. Eventual ICD placement

Non-sustained VT - brief, self-limited, asymptomatic

If CAD/LV dysfunction → risk factor for sudden death

a. No heart disease or asymptomatic → no treatment

b. Heart disease, recent MI, LVD → electrophysiology study

Post-MI: poor prognosis

Ventricular Fibrillation

Rate: cannot be determined

Rhythm: chaotic, irregular

P wave: none

PR interval: indiscernible

QRS: none

No T waves

Sudden unconsciousness and death, early morning

Cannot measure BP; absent heart sounds and pulse

1. Severe hypotension or LOC → synchronized cardioversion

2. Pulseless v-tach: immediate defibrillation and CPR

-If continued → 1 mg IV bolus epinephrine, then q 3-5 minutes

-Defibrillate q 30-60 seconds

-Refractory Vfib: IV amiodarone, followed by shock

If cardioversion successful: continuous IV infusion of effective drug, implantable ICD

Junctional Rhythms - not covered

Heart Blocks

A prolonged PR interval is >0.2 seconds (5 small boxes, or one large square)

First Degree

Obstruction at AV node incomplete; all impulses conducted but delayed

Causes: inferior MI, drug effect

Rate: varies

Rhythm: Regular (NSR, brady, or tachy)

P-wave: upright, uniform, one p-wave for each QRS complex

PR interval: prolonged, but all same length (>0.20 s)

QRS:  <0.12 s

Usually asymptomatic, patient typically an athlete

No treatment

Second Degree Type I (Wenckebach)

Site within AV node

Causes: vagal stimulation, ischemic heart disease, acute inferior wall MI

Drugs: BB, CCB, digitalis

Rate: varies

A: 60-100

V: <100, varies (faster than type II)

Rhythm: Irregular ‘grouped beating’

P-wave: normal shape and size, not every wave followed by QRS

PR interval: gets progressively longer until dropped QRS complex

QRS: <0.12 s

P:QRS ratio 3:2, 4:3, 5:4

Usually asymptomatic with irregular pulse w/ dropped beats

Resolves spontaneously - supportive care, D/C offending drugs

Vagal maneuvers produce a 2:1 AV block → 3:2 AV block (more cycles/series)

Temporary transthoracic or transvenous pacing → permanent pacing  

Second Degree Type II (Mobitz)

Site of block within His-purkinje system

Etiology: acute anterior wall MI, calcific aortic stenosis

Rate: varies

Rhythm: Regular or irregular

A: 60-100 (2-4 x ventricular)

V: <60, bradycardia

P-wave: Normal, more than 1 wave for each QRS

PR interval: constant, may be prolonged (usually normal)

QRS: <0.12 s

P:QRS ratio of 3:1, 4:1, 5:1

Presents with irregular pulse and occasional dropped beats, LOC

1. Shock if symptomatic

-Vagal maneuvers produce a 2:1 AV block → 1:1 AV block (eliminate or no effect)

2. Temporary transthoracic or transvenous pacing → permanent pacing

3. If asymptomatic, Atropine 0.5 mg IV

-If on BB, discontinue

Third Degree (Complete Heart Block)

All P-waves blocked at AV  node, ventricles won’t contract unless another failsafe mechanism kicks in

Due to lesion distal to His bundle

Etiology: CV surgery, congenital, trauma, CM, aortic stenosis, acute inferior wall MI, Lyme disease

Rate: varies (25-40)

Rhythm: Regular (NSR, brady, or tachy)

P-wave: normal

PR interval: inconsistent

QRS: >0.12 s (WIDE)

Presents with dizziness, palpitations, syncopal attacks, angina, CHF (SOB)

1. Temporary transthoracic or transvenous pacing → permanent pacing

2. Atropine 0.5 mg IV

3. Epinephrine IV drip 2-20 mcg/min OR Dopamine 2-10 mcg/min

R on T Phenomenon

Precursors for ventricular tachycardia or fibrillation, Torsades, and sudden death

Cause: hypoxia or hypokalemia

R wave falls on or near the T wave of preceding beat, representing a ventricular depolarization of an ectopic beat on preceding T wave

QT Prolongation (Long QT Syndrome)

Precursor to lethal arrhythmia with structurally normal heart

Ex. acquired (electrolytes, antibiotics, psych meds, ischemia), congenital

Electrolyte: hypokalemia, hypomagnesemia, hypocalcemia, Hypothyroidism

FQ and macrolides (Clarithromycin, Azithromycin)

SNRI, SSRI

All antipsychotics, TCAs and antifungals (fluconazole)

Adderall (Ritalin) for people with congenital long QT

Ranolazine, Quinidine

Lidocaine, Mexiletine

Dofetilide, Amiodarone, Sotalol

Propranolol

Presents with palpitations, Recurrent syncope, death

Pathologic prolongation of QT interval, less than 50% R-R

Normal QT varies with heart rate

0.39 male

0.41 female

Treat electrolyte abnormalities and D/C drugs that prolong QT

Torsades de Pointes (“Twisting of Lights”): rapid polymorphic V-tach

DANGEROUS: can lead to V-fib

Factors that prolong QT: congenital, TCAs, anticholinergics, electrolyte abnormalities, ischemia

Gradual change in amplitude and twisting of QRS around isoelectric line

Hypokalemia

Hypomagnesemia

Occurs spontaneously

IV magnesium, correct electrolyte abnormality

Remove offending drugs

Isoproterenol infusion and overdrive pacing after initial therapy

Recurrent - permanent pacemaker

Wolff-Parkinson-White Syndrome

A narrow complex SVT, accessory AV conduction pathway originating in the bundle of Kent

Rate: Tachycardia

Rhythm: Regular

P-wave: before each QRS, identical

PR Interval: <0.12 (short), decreased

QRS: >0.10 (wide)

2. Delta waves

1. Chest pain

-Sudden onset

-Without exertion

-Lasts 10-20 mins

-Can describe as chest heaviness

-Resolves spontaneously

-Recurrent episodes

2. Palpitations and SOB

3. Lightheadedness, chest pain lasting longer

4. Syncope

Tachycardic, hypertensive, cool, diaphoretic

Terminating acute episodes

-Vagal maneuvers

-AV blockade: IV adenosine 6-12 mg

1. Radiofrequency catheter ablation (preferred)

2. Adenosine 6 mg IV push, flush, 12 mg in 2 minutes: Antiarrhythmics to slow accessory conduction

3. AV node blocking drugs

-Avoid in acute setting

Avoid: CCB (Verapamil), Digoxin → both increase ventricular rates

Sinus Sick Syndrome

Abnormality of cardiac impulse formation that may be caused by an intrinsic disease of sinus node that makes it unable to pace-make or by extrinsic causes

MC: elderly patients with heart disease

May occur in heart surgery patients

Caused by scarring of heart’s conduction system

Worse with: digitalis, CCB, BB, sympatholytic agents, anti-arrhythmic drugs, aerosol propellant abuse

1. Sinus bradycardia, sinus arrest, sinoatrial block, alternating patterns of bradycardia and tachycardia, 2. Loss of P waves

1. Most asymptomatic

2. Non-specific: fatigue, irritability, memory loss, lightheadedness, palpitations

3. Syncope, presyncope, palpitations, dizziness, confusion, HF, palpitations, decreased exercise tolerance

1. Symptomatic - atrial or dual-chamber permanent pacemaker

-Provides effective relief of symptoms

-Lowers incidence of atrial fibrillation, thromboembolic events, heart failure, and mortality

-Digitalis can cause bradyarrhythmias in SSS

Complications: myocardial perforation, pneumothorax, wound hematoma, venous thrombosis, pacemaker lead failure, infection

Bundle Branch Blocks

Right Bundle Branch Block

Left Bundle Branch Block (Deep S)

V1

Notched R wave (RSR) or ‘bunny ears’

Small initial R wave

Wide, deep S wave

Primarily negative complex

V6

Deep S

Small Q wave, broad S wave

Broad R wave, often notched

No Q or S waves

Totally positive complex

A ST pattern of LBBB may obscure or mimic ST changes associated with ischemia or infarct

Sgarbossa’s Criteria for Acute Injury with LBBB

(1) Discordance is good, unless excessive (>5 mm) = 2 points (least predictive)

Appropriate discordance is expected → suspect acute injury

(2) ST depression (>1 mm) is concordant in V1-V3 = 3 points → suspect acute injury

(3) ST elevation (>1 mm) is concordant = 5 points → suspect acute injury

Axis

The Quadrant Method (most efficient)

Look at Leads I and aVF and identify the quadrant the axis is in based on the table below

The Isoelectric Lead (most precise)

Identify the limb lead that is most isoelectric (equal upward and downward deflection)

Identify the vector 90 degrees perpendicular to the isoelectric lead → calculate the QRS axis

Lead I

Lead AvF

Normal (0 to +90)

Upward

Upward

Right Axis Deviation (+90 to 180)

Downward

Upward

Extreme Right Axis Deviation (180 to -90)

Downward

Downward

Left Axis Deviation (-90 to 0)

Upward

Downward

Hypertrophy (Enlargement)

Atrial Hypertrophy

Lead

Right Atrial Enlargement

Look at first half of P wave

Left Atrial Enlargement

Look at second half of P wave

II

Tall, peaked P wave (P pulmonale)

Broad P wave (P mitrale)

V1

First deflection is largest

Last deflection is largest

Ventricular Hypertrophy

Lead

Right Ventricular Enlargement

Left Ventricular Enlargement

V1

Tall R wave

Deep S wave

V6

Deep S wave

Tall R wave

Rule of 35: verifies presence of left ventricular enlargement (LVH)

Measure depth of deepest wave in V1 or V2

Add height of tallest wave in V5 or V6

If sum is >35 mm and patient >35, criteria for LVE met

Largest R and Largest S > 45 mm in any precordial leads (V1-V6)

R wave in AvL > 11 mm

R wave in AvF > 20 mm

R wave in I and S wave in III > 25 mm

Infarction and Ischemia

Coronary Arteries of the Heart

RIP: RCA (right coronary artery) = Inferior + Posterior

LAL: LCA (left coronary artery) = Anterior + Lateral

Inferior Wall

II, III, AvF

Lateral Wall

I, AvL, V5-V6

Anterior Wall and Septum

V1-V4

Acute Injury

Old Infarction (Q waves)

Always give priority to ST elevation, if present

Significant Q Waves

1 mm wide (1 small box) or ⅓ QRS amplitude

Acute Injury

Anterior Wall Infarction

Leads: V1, V2, V3, V4

Q waves and ST elevation in V1 and V2

Inferior Wall Infarction

Leads: II, III, aVF

Lateral Wall Infarction

Leads: I, aVL, V5, V6

Posterior Wall Infarction

Acute Posterior Infarction = ‘ST Depression’

Posterior Wall MI: ST depression rather than elevation, upright T-wave, and tall, broad R wave (Q wave seen in reverse)

6. Other Findings

COPD

1. Multifocal Atrial Tachycardia

2. Small amplitude in EKG leads

3. Right axis deviation

Pulmonary Embolus

S1 Q3 T3

Lead I: large S wave

Lead II: ST depression

Lead III: Large Q wave in III with T wave inversion

V1-V4: T wave inversion

Transient RBBB

Hyperkalemia

Hypokalemia

Wide, flat P; Tall, peaked T wave, Wide QRS

Extreme: QRS very wide, no P wave

Flat T wave, U wave

Extreme: Prominent U waves

Hypercalcemia

Hypocalcemia

Short QT

Prolonged QT

Cardioversion vs. Defibrillation

Indications

Cardiac Pacemakers

- Delivers direct electrical stimulation to heart when heart’s natural pacemaker is unable to do so

Permanent - long term

Transcutaneous or transvenous - use external pulse generator that patient secures to waist with straps

-Sinus node dysfunction, also known as sinus sick syndrome (MC): with symptomatic bradycardia, HR <40 bpm, minimal symptoms with HR <30,

-Symptomatic heart block (mobitz type II and complete)

-Symptomatic bradyarrhythmias

-Tachyarrhythmias

Cardioversion

-Delivery of shock that is in synchrony with the QRS complex

-Purpose is to terminate dysrhythmias (PSVT, VT)

-An electrical shock during T wave can cause V-fib

A-Fib, atrial flutter

VT with a pulse

SVT

Defibrillation

-Delivery of a shock NOT in synchrony with QRS complex

-Purpose is to convert dysrhythmia to normal sinus rhythm

VT WITHOUT a pulse

V-fib

Automatic Implantable Defibrillator

Device that is surgically placed: when it detects a lethal dysrhythmia, it delivers a shock to defibrillate

Delivers a set number of shocks until the dysrhythmia is terminated

VT not controlled by medical therapy

V-fib

Pharmacologic Cardioversion

IV Ibutilide, Procainamide, Flecainide, Sotalol, Amiodarone

If electric cardioversion fails

Antiarrhythmics: “Some Bomb Pharmacology Class”

Class

Action

Indications

Contraindications

AE’s

Ia

Sodium channel blockers: higher affinity for open and/or inactivated state, slow down recovery

1. Decrease conduction velocity

2. Increase effective refractory period (slow transition from inactivated to resting, block re-entry circuits)

3. Raise threshold for impulse generation

SVT, V-tach

Prevention of V-fib

Symptomatic PVCs

MI, CAD

Quinidine (PO): Hypotension, diarrhea, thrombocytopenia, QT prolongation, SLE

Procainamide (IV): Hypotension, SLE

Ib

“ “

V-tach, prevention of V-fib

Symptomatic PVCs

HF, elderly

Lidocaine (cannot be used with corn allergy)

Lidocaine (IV): seizures, respiratory arrest, nervous, tremor, paresthesias

Mexiletine (PO): lightheaded, dizzy, nervous, ataxia, incoordination, tremor

Ic

“ “

Life-threatening V-tach or V-fib

Refractory SVT

Paroxysmal A-fib/Flutter

WPW

CHF, CAD - do not use in any heart abnormality

Flecainide: proarrhythmia, bronchospasm, leukopenia, thrombocytopenia, seizures

Black box: chronic A-fib

II

Beta-blockers: Block adrenergic receptors, blunting sympathetic effects

SVT, may prevent V-fib

Asthma, COPD

Bradycardia

AV block (chronic A-fib)

CHF/LVF

Esmolol

Propranolol: fatigue, impaired exercise, ED, chest pain, hypotension, bronchoconstriction, hypoglycemia

Metoprolol: bradycardia, impaired exercise, fatigue, ED, depression, chest pain

III

Potassium channel blockers

Blocks outward potassium channels, prolonging action potentials and increasing refractive period

Prolongs QT - monitor for QT prolongation

Refractory V-tach, ST

A-fib and flutter

Amiodarone: (IV) sustained VT, V-fib, (PO) A-fib, A-flutter, SVT, VT

Sotalol: A-fib

Dofetilide: A-fib, A-flutter

Amiodarone: pulmonary fibrosis, hypothyroidism, blue-gray skin, bradycardia, photosensitivity

Sotalol: bradycardia, bronchospasm, CHF, torsades

Dofetilide: liver injury, torsades

Ibutilide

IV

CCB: affect SA and AV nodes

SVT

Verapamil, Diltiazem

V

Adenosine: slows conduction time through AV node, interrupts reentry pathways

Digoxin: direct action on cardiac muscle and indirect action on CV system via ANS

SVT

Adenosine: headache, flush, SOB, chest pressure, nausea

Digoxin

Credits:

Dale Dubin

TrueLearn Questions

Question 1: A 76-year-old woman is hospitalized for altered mental status. Urinalysis shows >50 white blood cells per HPF and many bacteria. She is started on empiric antibiotics while urine cultures and sensitivities are pending. On the third day of hospitalization, she has an abnormal tracing on telemetry. Her past medical history is significant for myocardial infarction seven years ago and type II diabetes, for which she takes aspirin, metoprolol, lisinopril, metformin, and glipizide. Her pulse is 140 beats/minute, and blood pressure is 135/88 mm Hg. She is awake, alert, and fully oriented. She denies any lightheadedness, chest pain, or palpitations. A portion of her ECG is shown below. Which of the following is the next best step in the management of this patient?

Adenosine

Diltiazem

Procainamide

Transvenous pacing

Unsynchronized cardioversion

Explanation:The patient in this vignette has sustained monomorphic ventricular tachycardia (SMVT), which is defined by the following characteristics:(1)   Regular, wide QRS complex tachycardia at a rate of >100 beats/minute(2)   Consecutive beats have a stable QRS morphology(3)   Arrhythmia lasts ≥30 seconds or causes hemodynamic collapseThe treatment of SMVT depends on the degree of hemodynamic tolerance. For patients who are hemodynamically stable with SMVT, intravenous pharmacotherapy with an antiarrhythmic such as procainamide may be attempted prior to cardioversion. Amiodarone and sotalol have equal efficacy in terminated SMVT. Lidocaine has fallen out of favor due to less efficacy in comparison to the aforementioned drugs.Answer A: Adenosine is used to diagnose and treat narrow QRS complex supraventricular tachycardia (SVT), not ventricular tachycardia.Answer B: Diltiazem is incorrect. Diltiazem is a calcium channel blocker used for rate control in the atrial fibrillation with rapid ventricular response.Answer D: Transvenous pacing is indicated in the case of severe bradyarrhythmias causing hemodynamic collapse.Answer E: Patients with hemodynamically significant SMVT should be treated with immediate electrical cardioversion. Since this patient is asymptomatic, pharmacotherapy is the more appropriate initial step in management.Bottom Line: Hemodynamically stable sustained monomorphic ventricular tachycardia is first treated with intravenous pharmacologic therapy (procainamide, amiodarone, sotalol, lidocaine), prior to electrical cardioversion. Review the management of common arrhythmias, as they are frequently tested.

Question 2: A 50-year-old African American woman comes to the emergency room with a vague feeling of discomfort. She denies any loss of consciousness, chest pain, or diaphoresis. She has been compliant with her metoprolol and hydrochlorothiazide but has had decreased exercise tolerance. The physical examination is normal, except for mild edema bilaterally in each ankle. A portion of her ECG is shown below. Which of the following treatments is best for the following arrhythmia?A. AtropineB. Adenosine

C. AmiodaroneD. Electrical cardioversionE. Pacemaker placementExplanation:The above rhythm strip shows a Mobitz type 2 heart block. This rhythm has a fixed PR interval with the occasional dropped beat. This beat can progress to complete heart block, so the patient must be monitored closely in an ICU until a pacemaker can be implanted.Answer A: Atropine is used in resuscitation of a patient with bradycardia and asystole since it blocks acetylcholine and provides sympathetic stimulation to the heart.Answer B: Adenosine is used for patients with SVT since it acts on the AV node to stop any reentrant circuit.Answer C: Amiodarone is an anti-arrhythmic agent with a significant side effect profile. There is no need for an anti-arrhythmic in this case, as pacemaker is definitive treatment.Answer D: Electrical Cardioversion is always used in patients who are unstable with an arrhythmia or who are in ventricular fibrillation or tachycardia. This patient has a block, which does not respond to cardioversion.Bottom Line: Mobitz type II blocks consist of a fixed PR interval with dropped QRS complexes. Treatment of Mobitz II block always requires pacemaker placement due to possible progression to complete block.

Pancreatitis and Pancreatic Cancer

I can’t even stress to you how frequently PA students are tested over pancreatitis (acute and chronic) and pancreatic cancer. It seems to be one of those vague presentations that test writers take advantage of by placing in distractors (answers that seem right, but are in fact incorrect). This is meant to be a short, but hopefully helpful review of each of them, so that you are better prepared to tackle questions on these topics regardless of if they’re your in house exams during didactic, PAEA end-of-rotation exams, the PACKRAT, the PANCE, or the PANRE. I hope this helps you regardless of which avenue you find it useful. Good luck and make sure to check out TrueLearn’s free sample questions below! I’ll say, I loved their gastroenterology section the most. The vignettes were on point and difficulty wise - they were spot on with the EORs and PANCE-style questions.

Acute and Chronic Pancreatitis

Acute Pancreatitis

Inflammation of pancreas from prematurely activated enzymes → pancreatic autodigestion

Causes: ETOH (40%), gallstones (40%), post-ERCP, viral infection, drugs, scorpion bites, pancreatic cancer, hypertriglyceridemia, hypercalcemia, uremia

Blunt trauma (MCC in children)

Mild (most common)

- Abdominal pain, epigastric, radiates to back (50%), steady, dull, and severe

-Worse when supine and after meals

-Nausea, vomiting, anorexia

Signs

- Low grade fever, tachycardia, hypotension, leukocytosis

-Epigastric tenderness, abdominal distention

-Decreased/absent bowel sounds

-Hemorrhagic pancreatitis: Grey Turner’s sign (flank), Cullen’s Sign (periumbilical), Fox’s sign (inguinal ligament)

1. Serum amylase (MC) - nonspecific, absence does not r/o, 5xULN, normal 48-72 hours after

2. Serum lipase - more specific (3xULN)

3. LFTs - possible gallstone pancreatitis

4. Hyperglycemia, hypoxemia, leukocytosis

5. Ranson’s criteria: glucose, calcium, hematocrit, BUN, ABG, LDH, AST, WBC

6. KUB - r/o perforation

7. Abdominal U/S - identifies cause

8. CT scan (confirmatory) - most accurate

9. ERCP - severe with obstruction

1. Mild - Bowel rest (NPO), IVF, replete electrolytes, pain control (Fentanyl, Meperidine)

2. Severe - high mortality; ICU admit

-Enteral nutrition in first 72 h through NJ tube

Recurrence high in ETOH related

Complications:

- Pancreatic necrosis

- Pancreatic pseudocyst

Chronic Pancreatitis

Persistent, continued inflammation of pancreas → fibrosis and alteration of ducts = irreversible

Causes: chronic ETOH-ism

Other: hereditary, tropical, idiopathic

Severe epigastric pain, recurrent or persistent

-Nausea and vomiting

--Aggravated by drinking or eating

-Radiates to back

-Weight loss due to malabsorption, ETOH, diabetes

-Steatorrhea due to malabsorption

1. CT scan (first) - calcifications, normal does not r/o

2. KUB - pancreatic calcifications (95% specific)

3. ERCP (gold standard): “chain of lakes”

4. Serum amylase and lipase not elevated, other labs not helpful

5. Stool elastase - most sensitive and specific for pancreatic insufficiency (steatorrhea secondary to malabsorption)

1. Pain meds, NPO, pancreatic enzymes and H2 blockers, insulin, ETOH abstinence

2. Frequent, small volume, low fat meals

3. Surgery - pancreatico-

jejunostomy or pancreatic resection (Whipple’s)

Complications

-Narcotic addiction (most common)

-DM - loss of islets of Langerhans

-Malabsorption: late manifestation

-Pseudocyst

-CBD obstruction

-B12 malabsorption

-Effusions

-Pancreatic carcinoma

Pancreatic enzymes - inhibit CCK release, decreasing pancreatic secretions after meals

H2 blockers - inhibit gastric acid secretion, preventing degradation of enzyme supplements by gastric acid

Pancreatic Pseudocyst

Pancreatic Pseudocyst

Patients with chronic pancreatitis from alcohol usage or gallstones are at risk

10% occur after acute pancreatitis

Collection of fluid surrounded by granulation tissue

If it communicates with the pancreatic ductal system, it can contain digestive enzymes; does not contain epithelial lining (not cystic lesion of the pancreas)

1. Persistent abdominal pain, anorexia, or abdominal mass after pancreatitis

2. Jaundice or sepsis from infection (rare)

Physical exam

1. Tender abdomen

2. Palpable abdominal mass

3. Peritoneal signs suggesting rupture

4. Fever

5. Scleral icterus

6. Pleural effusion (common)

1. CT scan (standard)

2. ERCP - not for diagnosis, but useful for drainage

Labs

1. Serum amylase and lipase: elevated, limited use

2. Serum bilirubin and LFTs: elevated, limited use

3. Cyst fluid analysis: CEA, CEA-125, fluid viscosity, amylase (all low)

1. Supportive care only - MOST

2. Drainage for - complications, symptoms, possible malignancy

a. Percutaneous catheter drainage (preferred)

B. ERCP

C. Surgical Drainage (standard)

10% become infected, but can also rupture causing peritonitis or death

Poor prognostic factors: size of cyst and duration of presence

Outpatient monitoring: if stents placed, monitor with serial CT scans to observe resolution

Pancreatic Cancer

Pancreatic

Cancer

Most common in elderly patients (>60), African Americans

Anatomic location: pancreatic head (75%), body (20%), tail (5-10%)

RF: smoking, high fat diets, age >45, male gender, chronic pancreatitis, diabetes, heavy alcohol use, exposure to chemicals, first degree relative

Most adenocarcinomas (50%) involving head of pancreas

-Abdominal pain: vague and dull ache, epigastric, may radiate to back

-Painless Jaundice: most common with carcinoma of the head

-Weight loss; anorexia

-Recent onset glucose intolerance, but diabetes is mild

-Depression, weakness, fatigue

--Trousseau's sign: Migratory thrombophlebitis (10%)

-Courvoisier's sign: painless palpable gall in 30%

1. CT scan (preferred): pancreatic mass, dilated pancreatic and hepatic metastases, vascular involvement  

2. ERCP - most sensitive (confirms diagnosis); obtain sample for biopsy

3. MRCP - noninvasive, visualize hepatic and biliary symptoms, no tissue sampling

Tumor markers

1. CA 19-9 (more sens/spec)

2. CEA

1. Surgical resection with pancreatico-

duodenectomy  (Whipple’s procedure)

2. Chemotherapy: 5-FU and Gemcitabine

3. If unresectable - ERCP or PTC with stent placement

4. Most treatment is palliative care because of metastases

Prognosis: 5-year survival rate is 10%

1. A 45-year-old man is evaluated for a one-year history of severe chronic abdominal pain. The pain is located in the epigastric and left upper quadrant regions. Certain foods appear to precipitate the pain; however, it is unaffected by antacids. Associated symptoms include repeated bouts of loose steatorrhea and a 10 pound weight loss over the last 6 months. Three years ago he was hospitalized for acute abdominal pain. He smokes one pack of cigarettes per day and consumes 6-10 beers daily. His family history is significant for diabetes in his mother. On physical examination, he appears well. He does not have any scleral icterus.

Which of the following is most likely to confirm the diagnosis?

CA 19-9

D-xylose absorption test

HIDA scan

Serum amylase and lipase

Stool elastase

Explanation:

An alcoholic patient presenting with chronic abdominal pain and diarrhea is a classic case description of chronic pancreatitis. Chronic inflammation of the pancreas, most commonly secondary to alcohol or gallstones, is characterized by abdominal pain and symptoms of pancreatic insufficiency. Pancreatic insufficiency typically manifests first as exocrine dysfunction (i.e., fat malabsorption) with gradual progression to endocrine dysfunction (i.e., diabetes) if the insult continues. The diagnosis of chronic pancreatitis can be somewhat difficult to make. Stool elastase can be beneficial in diagnosing malabsorption secondary to pancreatic exocrine insufficiency. This test is the most sensitive and specific test for pancreatic insufficiency.

Answer A: CA 19-9 is a biomarker for pancreatic cancer. The most common presenting symptom of pancreatic cancer is painless jaundice. In contrast, this patient presented with severe chronic pain. While weight loss is associated with malignancy, the history of diarrhea does not fit a diagnosis of cancer as well as one of chronic pancreatitis.

Answer B: Although a D-xylose absorption test would demonstrate that the patient above is suffering from malabsorption, unlike stool elastase, it is not specific to the pancreas.

Answer C: HIDA scans are useful for evaluating the function of the gallbladder.

Answer D: Serum amylase and lipase may be modestly elevated but are more commonly normal due to the presence of significant fibrosis and only patchy inflammation in chronic pancreatitis.

Upper GI endoscopy would not be helpful here. This would be more useful in the diagnosis of upper GI diseases, such as peptic ulcer disease.

Bottom Line: Stool elastase can be used to diagnose chronic pancreatitis.

For more information, see http://emedicine.medscape.com/article/181554-overview

2. A 40-year-old man presents for a routine check-up. Physical exam is within normal limits. Labs show a triglyceride level of 1500-mg/dL, total cholesterol of 140-mg/dL and LDL of 100-mg/dL. His blood pressure is 140/90 and he smokes one-half-a-pack per day. He is at risk for pancreatitis due to his:

Hypertension

Smoking

LDL cholesterol level

Triglyceride level

Total cholesterol level

Explanation:

This patient has elevated triglycerides while the rest of the lipid profile is within normal limits. A high triglyceride level is a risk factor for pancreatitis. His blood pressure is on the border while his triglycerides are very elevated. Below is the typical appearance of acute pancreatitis on a CT scan. Answers A, C, & E: Hypertension and high cholesterol are risk factors for stroke. His LDL is within normal limits, thus his risk for coronary artery disease is low.

Answers A & C & E: Hypertension and high cholesterol are risk factors for stroke.  His LDL is within normal limits, thus his risk for coronary artery disease is low.

Answer B: This patient has only one risk factor for coronary artery disease, namely smoking.

Bottom Line: A high triglyceride level is a risk factor for pancreatitis. While this patient has high blood pressure, blood pressure should be measured on three separate occasions before diagnosing hypertension.

For more information, see: http://emedicine.medscape.com/article/181364-overview

3. A 30-year-old man presents with severe abdominal pain, nausea and vomiting for the last few hours. He was eating pizza and drinking beers with a few friends when the pain began. The pain radiates from his epigastrium directly to his back and is constant. He has never had pain like this before, and he states that he has no known medical problems. He drinks a few beers and smokes a few cigarettes with his friends during the weekend but denies using either consistently. His family history is significant for a father that died of a myocardial infarction at 45, and a grandfather with coronary artery disease. On examination, his temperature is 38°C (100.4°F), pulse is 115 beats/minute, respirations are 20 breaths/minute, and blood pressure is 105/65 mm Hg. There is severe pain on epigastric palpation and there are several xanthomas under his eyes. His laboratory values are shown below.

Leukocyte count 18,000 cells/mm3

Lipase 175 U/L

AST 70 U/L

ALT 55 U/L

Alkaline phosphatase 80 U/L   

Which of the following is the most likely cause of his symptoms?

Alcohol

Cigarette smoking

Factitious disorder

Gallstones

Hypertriglyceridemia

Explanation:

Although the most common causes of acute pancreatitis are gallstones and alcohol, this patient has a more rare cause - hypertriglyceridemia. His family history of a grandfather with coronary artery disease and a father with a early death from a myocardial infarction suggest he may have a form of familial hypertriglyceridemia. His xanthomas also suggest hypertriglyceridemia. This should be treated immediately to decrease his morbidity and help improve his pancreatitis. In the meantime, this patient requires abdominal imaging to view the pancreas and should receive fluids and bowel rest.

Answer A: Alcohol is a common cause of pancreatitis, but it is more often a result of chronic alcoholism not the social drinking this patient describes.

Answer B: Recent studies have documented a link between cigarette smoking and acute pancreatitis, but it occurs as a result of long-term, consistent usage, not the social smoking described by this patient.

Answer C: In factitious disorder, the patient fakes or causes a condition for primary gain of being taken care of in the sick role. This patient has pancreatitis, which he is not causing on his own.

Answer D: Gallstones are an extremely common cause of pancreatitis. Although this patient should certainly receive a right upper quadrant ultrasound to search for any stones, his chronic hypertriglyceridemia is a more likely cause. Gallstones usually present with right upper quadrant pain preceding the episode of pancreatitis, and the risk factors for gallstones are usually obesity, female sex, fertility, and age over 40.

Bottom Line: Hypertriglyceridemia is a known cause of pancreatitis.

Seizures, Headaches, and Migraines

Updated: 04/18/2016

Seizures, headaches and migraines are some of the most commonly occurring questions on the PACKRAT, EORE, PANCE, and PANRE. Since they also occur commonly in practice, you’ll definitely want to cover these topics thoroughly. Knowing the subtleties between each and the questions to ask is important not only for your understanding, but so you can treat the patient accordingly with the most appropriate therapy.

While Neurology only makes up 6% of the PANCE, knowing topics like this well can mean the difference between passing and not passing. As I have stated before, one of the best ways to prepare for your exams is through quality question banks and study guides. TrueLearn has introduced an incredible opportunity to work with the PA-student and PA community to help us excel in our didactic education and clinicals, and on our boards. See below for our second post discussing Seizure Disorders and Headaches and Migraines.

Remember from last month that TrueLearn’s SmartBanks include specialized medical content crafted to mirror End of Rotation Exams (EORs), the PACKRAT, the PANCE and the PANRE. This means that the best test writers have come together to write questions that not only get your juices flowing, but challenge you to think critically - the most important characteristic of great PAs.

Visit TrueLearn.com/Physician-Assistant/ today to learn more about their physician assistant products.  

Disclosure: I am not an employee of TrueLearn.

Seizure Disorders - sudden abnormal discharge of electrical activity

Epilepsy - syndrome of recurrent, idiopathic seizures

In seizures, duration of unconsciousness tends to be longer than in syncope (momentary)

In syncope, bladder control is retained, but lost in seizures

Causes: four Ms and four Is

Metabolic and electrolyte disturbances - hyponatremia, water intoxication, hypoglycemia and hyperglycemia, hypocalcemia, uremia, thyroid storm, hyperthermia

Mass lesions - brain mets, primary brain tumors, hemorrhage

Missing drugs

Non-compliance with anticonvulsants (most common reason)

Acute withdrawal from alcohol, benzos, barbituates

Miscellaneous

Pseudoseizures - psychiatric in origin

Eclampsia

Hypertensive encephalopathy

Intoxication - cocaine, lithium

Infection - septic shock, bacterial or viral meningitis, brain abscess

Ischemia - stroke, TIA (common in elderly)

Increased ICP due to trauma

Diagnosis

If known epileptic → check anticonvulsant levels

If first seizure

CBC, CMP (LFTs), blood glucose, renal function tests, serum calcium, urinalysis

EEG: most helpful diagnostic test, abnormal pattern is not diagnostic alone

CT scan of head: r/o structural lesions

MRI of brain with and without gadolinium: more sensitive than CT for structural changes

LP/blood cultures if febrile

Pregnancy test - before initiating anticonvulsants!!!

Treatment

ABCs first, secure airway and roll patient to side

Known epileptics

Check for non-compliance of anticonvulsant, check levels

If persistent with monotherapy, increase dose of first anticonvulsant until signs of toxicity appear → add second drug if seizures uncontrolled

If controlled → continue regimen x 2 years, then taper

First seizure

EEG with neurology consult

Anticonvulsant therapy

If normal EEG, recurrence low (15%) compared to abnormal EEG (41%)

Do not treat patients with single seizure - start antiepileptics if EEG abnormal, MRI abnormal or status epilepticus

Partial Seizures (70%), begins in one part of brain (temporal) and produces symptoms referable to region of cortex involved

May evolve into generalized seizures (called Secondary Generalized)

Simple

Consciousness intact

Seizure - localized, but may evolve

May involve transient unilateral clonic-tonic movement

EKG: localized disturbances

1. Phenytoin and carbamazepine

2. Alternatives - phenobarbital, depakote, primidone

Complex

Consciousness impaired

Postictal confusion

Automatisms (last 1-3 mins): purposeless, involuntary, repetitive movements (lip smacking, chewing)

Olfactory and gustatory hallucinations

1. Phenytoin and carbamazepine

2. Alternatives - phenobarbital, depakote, primidone

Generalized Seizure - loss of consciousness; disruption of electrical activity in entire brain

Tonic Clonic (Grand Mal)

Bilaterally symmetric & without focal onset

-Begins with sudden LOC, “falls to ground”

-Tonic phase: rigid, trunk and limb extension occurs, may become apneic

-Clonic phase: muscular jerking of limbs and body for 30 seconds

-Patient becomes flaccid & comatose before regaining consciousness

-Postictal confusion & drowsiness, lasts hours (mean: 10-30 mins)

Other features: tongue biting, vomiting, apnea, incontinence (feces, urine)

EKG: generalized high amplitude, rapid spiking

1. Phenytoin and carbamazepine

2. Alternatives - phenobarbital, depakote, primidone

Absence (Petit Mal)

-School aged children, resolves as you age

-Disengage from current activity and “stare into space” - then returns to activity

-Patient looks “absent minded” during episodes which are confused with “daydreaming”

-Brief (lasts few seconds), but quite frequent (100 times/day)

-Impairment of consciousness but no loss of postural tone or continence, and no postictal confusion

-Minor clonic activity (eye blinks, head nodding, 45%)

EKG: spike and wave activity

1. Ethosuximide

2. Depakote (valproic acid)

Secondary Generalized

Partial seizures that evolve into generalized seizures

Status Epilepticus - prolonged, sustained unconsciousness with persistent convulsive activity in seizing patient lasting longer than 30 minutes OR 2+ sequential seizures without full recovery of consciousness between seizures.

Medical emergency - mortality is 20%

May be caused by poor compliance with meds, alcohol withdrawal, intracranial infection, neoplasm, metabolic disorder, drug overdose

Management: establishing an airway, giving IV diazepam, IV phenytoin, and 50 mg dextrose

Resistant cases: IV phenobarbital

Migraines, Tension Headaches, Cluster Headaches

Aggravators of migraines: menstruation, stress, anxiety, lack of sleep, drugs/foods (chocolate, cheese, alcohol, smoking, OCPs), weather changes

Visual aura in migraine: bilateral homonymous scotoma; bright, flashing, crescent shaped images with jagged edges appear on a page, obscuring the underlying print, lasts 10-20 minutes

Migraines with aura (15%)

“classic migraine”

Autosomal dominant with incomplete penetrance

Serotonin depletion

Women > Men

(+) family history

1. Visual aura: flashing lights, scotomata, visual distortions

1. Acute migraines

--NSAIDs, Tylenol, DHE or a Triptan

--DHE (5-HT1) agonist: highly effective

--Sumatriptan (5-HT1 agonist): rapid and effective, 1-2 times/week

2. Prophylaxis

--Avoid precipitants

--TCAs and Propranolol (most effective)

--Verapamil, Depakote, Methysergide

Migraines without aura (85%) “common migraine”

1. Prodromal phase (30%)

-Excitation or inhibition of CNS: elation, excitability, increased appetite or craving for foods, depression, irritability, sleepiness, fatigue

2. Severe, throbbing, unilateral headache

-Lasts 4-72 hours

-Generalized over entire head, lasting for days

-Aggravated by coughing, physical activity, or bending down

-”throbbing, dull, achy”

3. Nausea, vomiting (90%), photophobia, increased sense of smell

Menstrual migraines

Occurs 2 days before menstruation and last day of menses, estrogen withdrawal

--NSAIDs

Estrogen supplementation

Status migrainosus

Lasts >72 hours and does not resolve spontaneously

Tension Headaches

Unknown cause

Worsens throughout the day

Precipitants: anxiety, depression, stress

1. Pain - steady, aching, “vise-like” and encircles entire head (tight band-like), generalized but most intense around neck or back of head

2. Tightness in posterior neck muscles

Find causal factors, evaluate for depression or anxiety

Reduce stress

Mild/Mod: NSAIDs, Tylenol, ASA

Severe: migraine meds appropriate

Cluster Headaches

Rare

Middle-aged men

1. Episodic (90%) - last 2-3 months, with remissions of months to years

2. Chronic cluster headaches (10%) - last 1-2 years, headaches do not remit

1. Excruciating periorbital pain (“behind the eye”) - almost always unilateral

2. Deep, burning, searing, or stabbing pain

3. Ipsilateral lacrimation, facial flushing, nasal stuffiness/discharge

4. Begins few hours after patient goes to bed, lasts 30-90 minutes, awakens from sleep (daytime cluster headaches occur)

5. Occur nightly 2-3 months, then disappear

6. Worse with alcohol and sleep

1. Acute attacks

a. Sumatriptan (Imitrex)

b. O2 inhalation

2. Prophylaxis

Most responsive to Verapamil

Ergotamine, methysergide, lithium, steroids

Resolution of headaches within 1 week

TrueLearn’s Neurology Sample Questions

Question 1: A 45-year-old male is brought to the emergency department by ambulance after having a witnessed seizure. He is currently alert, but not oriented to himself or his surroundings. After his initial assessment, he begins to seize violently. He is given 5mg of midazolam intravenously yet continues to seize. An additional 10 mg of midazolam is administered intravenously, yet the patient continues to shake violently. Vitals reveal a blood pressure of 190/100 mmHg, a heart rate of 130/min, a respiratory rate of 44/min, and a room air oxygen saturation of 88%. The most appropriate course of action is

call for a stat neurology consultation

continue using benzodiazepines intravenously until his seizure stops

prepare to intubate the patient using propofol as the induction agent

provide bag-valve-mask ventilation until his seizure stops

roll him on his side to prevent aspiration

Explanation:

This is an example of status epilepticus (SE). Current definition of SE is more than 30 minutes of continuous seizure activity, or two or more sequential seizures without full recovery of consciousness between seizures. This patient had two sequential seizures without clearing from his post-ictal state, followed by continued seizure activity following high dose benzodiazepines. Benzodiazepines are the first line treatment for seizures. When this fails, one must resort to the ABC’s of patient care. This patient has no ability to control his airway if he continues to seize. Immediate recognition of this is critical. Intubation is indicated for airway protection. Propofol is the induction agent of choice because it is a powerful anti-epileptic drug (AED) as well as a commonly used induction agent for rapid-sequence-intubation.

Answer A: Call for a stat neurology consultation is incorrect. The patient needs immediate stabilization of his airway. Remember the ABCs. Airway, breathing, and circulation come before all else. Once the patient is stabilized (via intubation and sedation), you have a high priority to call neurology for continuation of care.

Answer B: Benzodiazepines are the first line treatment for seizures, and are effective in the majority of cases. This patient has failed high dose treatment with a benzodiazepine, and continues to seize. Therefore a different medication should be used. Frequently used alternatives are phenobarbital and propofol, which are both powerful medications used to suppress seizure activity. When using either of these medications, the respiratory drive will be decreased and therefore intubation is usually required.

Answer D: Bag-valve-mask (BVM) ventilation will not help this patient. In fact, forcing breaths into this patient will likely only induce aspiration and possibly produce aspiration pneumonitis. His oxygen saturation should be maintained by simple nasal cannula or non-rebreather mask that will not force air into the trachea or esophagus.

Answer E: This patient requires immediate protection of his airway. Rolling him onto his side may transiently help prevent aspiration, but has done nothing to treat the underlying pathology. A patient in SE can inhale saliva, blood and gastric contents regardless of the way they are positioned, thus making this answer incorrect.

Bottom Line: Status epilepticus is defined as more than 30 minutes of continuous seizure activity or two or more sequential seizures without full recovery of consciousness between seizures. Management includes high dose benzodiazepines and management of the ABCs.

TrueLearn Insight : Remember the ABCs in all patients who are critically ill. You will have distractions and other management possibilities. When in doubt, be aggressive about protecting the patient by ensuring they have adequate airway protection/patency, spontaneous breathing, and adequate circulation. Do not move on until these are stable.

For more information, see:

Arif H, Hirsch L. Treatment of Status Epilepticus. Semin Neurol 2008;28:342–354. http://criticalcaremedicine.pbworks.com/f/Treatment+of+Status+Epilepticus.pdf

Ayala C, Spellberg B. Boards and Wards. 4th Ed. Philadelphia, PA; Lippincott Williams & Wilkins; 2010: 378-379. "Status epilepticus" on Medscape. http://emedicine.medscape.com/article/1164462-overview.

Question 2: A 46-year-old man with a history of hypertension visits your office and complains of frequent headaches over the past year. The pain generally begins behind the right eye and expands throughout his skull as time progresses. The pain is constant, severe, and persists for hours or days. The headaches are not preceded by visual perceptions of flashing lights or zigzag lines. He does not experience muscle weakness, difficulty speaking, or dizziness. Occasionally the patient experiences nausea during the headaches, but he does not vomit. Caffeine sometimes helps diminish the pain. He is most comfortable lying in a dark, quiet room until the pain subsides. On physical examination, his heart rate is 90 beats/minute, respiration rate is 12 breaths/minute, and blood pressure is 182/96 mm Hg. His neurological exam is benign and non-focal. Other than a chronic cough that has improved since he stopped taking his blood pressure medication, the patient has no other medical problems or symptoms. Which of the following would be the best prophylactic treatment option?

Captopril

Losartan

Propranolol

Sumatriptan

Venlafaxine

Explanation:

The patient’s headaches are consistent with common migraine, also known as migraine without aura. The absence of preceding visual disturbances (zigzag lines, flashing lights) or motor weakness excludes the diagnosis of migraine with aura. The absence of dizziness or difficulty speaking generally excludes basilar migraine. Beta-blockers such as propranolol are often used for migraine prophylaxis. Propranolol is also a good choice considering this patient has a history of hypertension and demonstrates elevated blood pressure on exam. He has been non-compliant with his previous antihypertensive, likely an ACE inhibitor (angiotensin converting enzyme inhibitor), which elevates bradykinin levels and can lead to chronic cough.

Answer A: Captopril (ACE inhibitor) is likely similar to his previous hypertension medication and would cause his cough to return; additionally, it is not effective for migraine.

Answer B: Losartan (angiotensin receptor blocker) is effective against hypertension but would not be useful for migraine.

Answer D: Sumatriptan is very effective for migraine headaches, but as this patient also suffers from hypertension, propranolol is a better choice. It also would be a good abortive therapy but is not effective as prophylaxis.

Answer E: Venlafaxine has gained recognition for its efficacy with migraines, but it generally is not used as a first-line therapy unless the patient also suffers from a depressive disorder.

Bottom Line: In patients with migraine and uncontrolled hypertension, either a beta-blocker (propranolol) or calcium channel blocker (verapamil) would be the most logical medication to prescribe as each demonstrates efficacy in both conditions.

TrueLearn Insight : 1) Imaging is generally unnecessary in patients with headache unless there is focal neurological change, suspicion of acute intracranial process, or suspicion of basilar migraine. 2) Although caffeine can help alleviate symptoms for some migraine sufferers, its use can also contribute to migraine headaches and hypertension. For more information, see www.uptodate.com "Preventive treatment of migraine in adults"

Question 3: A 45-year-old man is pacing in the emergency department waiting room and complaining of headache. He says that this is the fifth headache he has had this week, and he rushed to be seen because the last four went away before he could get to the doctor. The pain is 8/10 in severity and it feels “like being stabbed in the eye,” always on the right. He says he had pain like this several years ago when he had a series of severe headaches over the period of about a month, but they had gone away. He has tried taking aspirin, ibuprofen, and acetaminophen but does not feel they have helped. His past history is significant for an inguinal hernia that was repaired seven years ago. His mother suffers from acute angle-closure glaucoma and migraine and his father died of a myocardial infarction at the age of 47. He does not smoke and drinks alcohol occasionally. On examination his right eye is injected and there is right-sided ptosis. Fundoscopic examination is normal. Which of the following is the next best step in management?

Head CT

High-flow oxygen

Intranasal sumatriptan

Lithium carbonate

Lumbar puncture

Explanation:

The patient’s history and exam are classic for cluster headache (severe unilateral stabbing pain, with injection and lacrimation of the ipsilateral eye, often with ptosis and miosis), which is treated acutely with high-flow oxygen.

Answers A and E: He does not need a head CT or lumbar puncture as the diagnosis is clear and there is no evidence of acute intracranial process.

Answer C: Intranasal or injected sumatriptan is appropriate after initiating oxygen therapy.

Answer D: Lithium carbonate has been suggested as a preventive medication for cluster headache but is not used to abort an acute attack.

Introducing TrueLearn

Updated: 03/17/2016

At the PAEA Summit I recently attended in Washington D.C. I learned that PA students and practicing PAs should understand that even once we graduate, we will always be a student. Continuous learning is an expectation not just of our peers or NCCPA, but of our employers as well, and our colleagues (physicians and NPs). Collectively, we must work to ensure we are practicing at the top of our career, implementing the best practices and presenting the most up-to-date information to our patients. One colleague put it plainly, “either be at the table, or be on it.” This can be interpreted in many ways, but I believe that regular review of content keeps us competitive.

Over the next 3 months, I will be selecting topics that are most commonly tested by the NCCPA and PAEA for exam preparation. TrueLearn, which provides next generation question banks (called SmartBanks), will provide free practice questions on these topics to provide insight into their test preparation expertise. One of the best ways to prepare for your exams is through quality question banks. TrueLearn has introduced an incredible opportunity to work with the PA-student and PA community to help us excel in our didactic education and clinicals, and on our boards. Moving forward, I am pleased to announce TrueLearn to the table of exam preparation for PAs from the start of your education. See below for our first post discussing Heart Murmurs. This topic is important as Cardiology makes up 16% of the PANCE and PANRE exams.

SmartBanks, brought to you by TrueLearn, the nation’s most trusted test preparation, provide the highest level of test readiness available today.Their products have served up over 39 million practice questions in 2015 alone, achieving an 11% score improvement after using their SmartBanks. TrueLearn’s SmartBanks have been utilized for USMLE, COMLEX, and specialty board exams in general surgery, anesthesiology, emergency medicine, family medicine, pediatrics, OB/GYN, internal medicine, and psychiatry. These exams are written by the nation's leading specialists and are used by most medical students and residents in preparation for shelf (clinicals) and board exams.

TrueLearn’s SmartBanks include specialized medical content crafted to mirror End of Rotation Exams (EORs), the PACKRAT, the PANCE and the PANRE. Why stop there? Use these exams to help you prepare for Certificates of Added Qualification (CAQ) - the limits are endless!

Visit TrueLearn.com/Physician-Assistant/ today to learn more about their physician assistant products.  

TrueLearn’s SmartBanks provides:

An accurate reflection of what you can expect on test day, both in regard to content and difficulty, so you can be rest assured you are prepared

A realistic test interface that closely mimics features provided for your EOR, PANCE, or PANRE. Alas, a testing platform that you can utilize from PA student on clinical rotations to clinician.

Board-style vignettes reflective of the EOR, PANCE and PANRE

Explanations with updated references, learning points

User-friendly software with easily accessible IT support for questions or concerns with quick 24-48 hour response

Adaptive performance analytics with personalized learning - fit to meet your weaknesses and allowing you to see where your strengths exist so you can focus your learning

Comparative analysis to your nationwide peers on individually created exams and questions

Train more effectively and monitor your progress as you go with a chart of your performance  

No more purchasing question banks with questionable validity - questions are written by PAs and MD/DOs and tested for accuracy, ensuring the level of difficulty will prepare you for test day

Prepare, assess, and improve your performance from home or on the go using the mobile app available on all smart devices

Disclosure: I am not an employee of TrueLearn.

Heart Murmurs

Key features

Description

Radiation

Other Clues  

Mitral Valve Prolapse: Regurgitant flow across mitral valve

Decreased left ventricular volume results in earlier prolapse and click heard earlier in systole, closer to S1

Increased left ventricular volume results in delayed prolapse, click heard later in systole

Mid-systolic click followed by a mid-to-late systolic murmur and loud S2

“click” is caused by prolapse of leaflets into left atrium and tensing of mitral valve apparatus

Maneuvers that increase left ventricular end diastolic volume (preload): squatting from seated or standing position

Maneuvers causing delay in prolapse: handgrip, standing from seated position, valsalva

Leads to mitral regurgitation

Predisposed to infective endocarditis

ADA no longer recommends prophylactic antibiotics for MVP

Mid-systolic (HAPI) Murmurs

Key features

Description

Radiation

Other Clues  

Hypertrophic Cardiomyopathy

Will cover this topic at a future date

Aortic Stenosis

Paradoxical split S2

Elderly, syncopal episodes

Crescendo-decrescendo harsh systolic ejection click radiating to carotids

Best heard on right

Brisk upward deflection of carotid

Base of heart

Severe: can be heard near carotid arteries

EKG: Left ventricular hypertrophy

Pulmonary Stenosis

Congenital disorder

Left sided HF: DOE, jugular pulsation, parasternal lift

Preceding systolic sound during expiration

Systolic murmur heard best at 2nd-3rd LICS, radiates to left shoulder

EKG: right axis deviation

Innocent Murmur

Will cover this topic at a future date

Holosystolic (MTV) Murmurs

Key features

Description

Radiation

Other Clues  

Mitral Regurgitation

Chronic mitral regurgitation seen in cases of acute rheumatic fever, but presents in first-second decade

High-pitched, blowing

Holosystolic murmur radiating to left sternal border

Apex (best) → Axilla

Reduced with valsalva

EKG: left axis deviation or LVH

Tricuspid Regurgitation

S3 may be present

Holosystolic murmur heard best at right sternal border, 5th ICS

NO EJECTION CLICK

Opening snap + diastolic murmur

Left sternal border

Increased with inspiration

EKG: right axis deviation

Ventricular Septal Defect (VSD)

Most common of all congenital heart defects

Depends on size of defect - from asymptomatic to CHF

Systolic murmur at LLSB

Diastolic (ARMS) Murmurs

Key features

Description

Radiation

Other Clues  

Aortic Regurgitation

Younger pt with h/o Marfan’s syndrome

or older patient  

High-pitched Blowing or rumbling diastolic decrescendo-crescendo (“V”) murmur heard at left sternal border or apex of heart

Bounding “water hammer” pulse

Classic: diastolic murmur at RSB due to backflow of blood across aortic valve

Rumbling sound at apex (Austin Flint Murmur) - retrograde blood across aorta mixes with anterograde blood from left atrium

Mitral Stenosis

Enlarged left ventricle

Common after rheumatic fever

Hemoptysis, presents in 30-40s

(1) Loud first heart sound: wide closing excursion of leaflets

(2) Prominent P2 of second heart sound (split S2): elevated pulm-art pressures

(3) Opening Snap: sudden tensing of leaflets after they’ve completed their opening excursion

(4) Mid-diastolic rumble - increased flow across stenotic MV during atrial contraction

Opening snap followed by low pitched diastolic rumble

Leads to pulmonary hypertension and heart failure → high LA pressures = high pulmonary vasculature and right heart pressures

Valvular Heart Disease

Aortic Stenosis - narrows valve opening, impeding the ejection function of the left side of the heart (most common valvular disease in US)

Thready carotid pulse

Aortic Regurgitation (insufficiency) - volume overloading due to retrograde blood flow into the left ventricle

Bounding pulses and wide pulse pressures

Mitral Stenosis - impedes blood flow between left atrium and ventricle

Mitral Regurgitation (insufficiency) - retrograde blood flow and volume overload of the left atrium

Mitral valve prolapse - may be asymptomatic, but associated with MR; mostly thin females with minor chest wall deformities, midsystolic clicks, and late systolic murmur

Most common causes of mitral/aortic valve disorders are congenital defects; other causes include rheumatic heart disease, connective tissue disorders, infection, sensile conditions

Most common presenting symptoms: dyspnea, fatigue, decreased exercise tolerance

Other: Cough, rales, paroxysmal nocturnal dyspnea or hemoptysis, hoarseness

Physical exam - heart murmur +/- palpable thrill  

Diagnostic Studies

EKG - not useful for specific diagnosis → shows chamber hypertrophy

CXR

Aortic → left sided atrial enlargement, ventricular hypertrophy

Mitral → atrial enlargement only

Echo (transesophageal) and cardiac cath → definitive

Treatment

Surgical repair or replacement of defective valve

Good exercise tolerance → diuretics and vasodilators for pulmonary congestion and digoxin or BB for dysrhythmias

Anticoagulant therapy for thromboemboli prophylaxis

Antibiotics to prevent endocarditis and recurrent rheumatic fever

Location

Radiation

Intensity

Pitch/Quality

Aids to Hearing

Associated findings

Timing

Aortic Stenosis

2nd Right-ICS

Neck and LSB

Loud with a thrill

(Grade 4-6)

Medium/

Harsh

Patient sitting and leaning forward

Midsystolic

Aortic Regurgitation

2nd-4th Left-ICS

Apex and RSB

Grade 1-3

High pitch/

Blowing

Patient sitting and leaning forward

Full exhalation

Mid-systolic or Austin Flint murmur suggests large flow;

arterial pulses large and bounding

Systolic (soft) and decrescendo in early diastole

Mitral Stenosis

Apex

Little/None

Grades 1-4

Low pitch

Patient in LLD

Full exhalation

S1 accentuated;

opening snap follows S2

Mid-Diastolic

Mitral Regurgitation

Apex

Left axilla

Soft to loud

Medium to high pitch;

Blowing

N/A

S2 decreased;

apical impulse prolonged

Pansystolic

Tricuspid Regurgitation

LLSB; holosystolic

Right sternum and xiphoid area

Variable

Medium;

Blowing

Increases with inspiration

JVP elevated

Pansystolic

Pulmonic Stenosis

2nd-3rd Left-ICS;

Mid-systolic

Crescendo

-Decrescendo

Left shoulder and neck

Soft to loud, possibly associated with thrill

Medium;

Harsh

N/A

Early pulmonic ejection sound (common)

Mid-Systolic

Mitral Valve Prolapse

Late systolic murmur

Mid-systolic

Tricuspid and Pulmonic Valve Disorders

Present during early infancy or childhood; adults present with stenosis from rheumatic scarring or connective tissue disease

Tricuspid regurgitation is intrinsic or functional

In all cases, right sided pressure overload → right sided cardiomegaly, systemic venous congestion, and right sided heart failure

Clinical features: exercise intolerance

JVD, peripheral edema, hepatomegaly

Diagnostic Studies

CXR: prominent R-heart border, dilation of SVC

EKG: right axis deviation, p-wave abnormalities with R-atrial enlargement, prominent R and deep S waves of RVH

Treatment

Sodium restriction, diuretic therapy

Surgical repair, valvuloplasty or replacement

Cyanotic Defects

Tetralogy of Fallot

6-10%

Crescendo-decrescendo holosystolic at LSB, radiates to back

1. Right ventricular hypertrophy

2. Pulmonic Stenosis

3. Overriding aorta

4. VSD

Tet-spells: irritability, tachypnea, cyanosis worse with exertion (feeding or intense crying)

Reduced with squatting: increases SVR

R → L shunting

Cyanosis, blubbing, increased RV impulse at LLSB,

Loud S2

Polycythemia; tet spells (hypercyanotic) include extreme cyanosis, hyperpnea, and agitation

EMERGENCY

Pulmonary Atresia

1-3%

Depends on presence of tricuspid regurgitation

Cyanosis with tachypnea at birth, tachypnea without dyspnea, hyperdynamic apical pulse, Single S1/S2

Sudden onset severe cyanosis and acidosis

EMERGENCY

Indomethacin

Hypoplastic Left Heart Syndrome

7-9%

Variable; not diagnostic

Shock, early heart failure, respiratory distress

Single S2

More often in males, 25% of cardiac death before age 7

Transposition of the great Vessels

5-7%

Systolic murmur if associated with VSD; systolic ejection murmur if associated with pulmonary stenosis

No exchange between right and left circulation

Cyanosis in newborn (MC)

Tachypnea without respiratory distress

If large, sx of CHF and poor feeding

Single loud S2

Absent LE pulses if aortic arch obst

Prostaglandin!!

Non-Cyanotic Defects: All Ventricles Provide Circulation (AVPC)

Atrial Septal Defect

7% of all defects

Cause: patent foramen ovale

Systolic ejection murmur at 2nd LCIS

Early to mid systolic rumble

Failure to thrive, fatigue

RV heave, wide fixed split S2

VSD

Most common of all congenital heart defects

Systolic murmur at LLSB

Depends on size of defect - from asymptomatic to CHF

Outlet VSDs more common in Japanese and Chinese

PDA

12-15% of significant congenital heart disease; higher in premature infants

Continuous (machinery) murmur

Wide pulse pressure; hyperdynamic apical pulse

Coarctation of the Aorta

Systolic, LUSB and left scapular area; may be continuous

Infants - CHF

Older children - systolic hypertension or new murmur or underdeveloped lower extremities

Differences between arterial pulses and blood pressure in UE/LE is pathognomonic

TrueLearn’s Sample Questions

Question 1: A 37-year-old woman presents for evaluation of progressive fatigue and shortness of breath. She immigrated to the United States from Cambodia when she was 17-years-old. She denies fever, night sweats, and weight loss. She does note occasional blood tinged sputum. She quit smoking 10 years ago but previously had smoked one pack per day for 10 years. She does not drink and denies any history of illicit or intravenous drug use. On exam her temperature is 37.0 C (98.6 F), pulse is 80 beats/minute, respirations are 16 breaths/minute, and blood pressure is 113/82 mm Hg. She is thin and appears fatigued but is in no apparent distress. There is a pink-purple papular and patch-like rash on her face. There are prominent a waves on examination of her neck. Lungs are clear auscultation. There is 1+ edema in the lower extremities bilaterally.

Which of the following murmurs is most likely present on cardiac exam?

A) Continuous, machine like murmur heart at the left upper sternal border

B) High-pitched, blowing, early diastolic murmur

C) High-pitched blowing, holosystolic murmur heard best at the apex

D) Loud first heart sound, S2, then an opening snap following by a mid-diastolic rumble

E) Systolic ejection click, followed by a crescendo-decrescendo murmur

Explanation:

This patient has mitral stenosis, the severity of which has led to pulmonary hypertension and heart failure. Her immigration status from a medically underserved area of the world puts her at higher risk of having untreated group A streptococcal infection as a child. The consequences of untreated infection include acute rheumatic fever and subsequent development of mitral stenosis, which usually presents in the 3rd or 4th decade of life.

The murmur associated with mitral stenosis includes the following components:

(1)  Loud first heart sound – due to wide closing excursion of the leaflets

(2)  Prominent P2 of second heart sound – P2 is accentuated due to elevated pulmonary artery pressures

(3)  Opening snap – caused by the sudden tensing of the leaflets after they’ve completed their opening excursion

(4)  Mid-diastolic rumble – due to increased flow across the stenotic mitral valve during atrial contraction

The additional findings on her exam can also be explained by this valvular abnormality. Mitral stenosis results in chronically elevated left atrial pressures which, over time translate into elevated pulmonary vasculature and eventually right-heart pressures. Hemoptysis is secondary to elevated pulmonary pressures. Prominent a wave on neck examination indicates elevated right atrial pressure. Her pinkish-purple facial rash (“mitral facies”) is secondary to reduced cardiac output and vasoconstriction seen in severe chronic mitral stenosis.

Answer A: This choice describes the murmur of patent ductus arteriosus. This is unlikely to be present in an adult as it typically closes prior to birth and is corrected early in life if present at birth.

Answer B: This choice describes the murmur of aortic regurgitation, which is associated with pulsus parvus et tardus. This most commonly occurs in older adults or in younger patients with a history of Marfan's disease.

Answer C: This choice describes the murmur of mitral regurgitation. Chronic mitral regurgitation is seen in cases of acute rheumatic fever but usually presents in the first or second decade of life. Hemoptysis is seen more often with mitral stenosis, not mitral regurgitation.

Answer E: This choice describes the murmur or aortic stenosis, which is most commonly seen in elderly patients, and is associated with syncopal episodes and brisk upward deflection of the carotid pulsation. While biscuspid aortic valve is associated with aortic stenosis in younger patients, mitral stenosis is more likely given her demography history and physical exam findings.

Bottom Line: The murmur of mitral stenosis is described as a loud first heart sound, a split S2 with prominent pulmonic component, following by an opening snap and mid-diastolic rumble.

Question 2: A 56-year-old man presents to the physician’s office with complaints of fatigue and shortness of breath on exertion that began six weeks ago. He denies cough, weight loss, unexplained fevers, chest pain, palpitations, or leg swelling. He drinks red wine once a week and smoked one pack of cigarettes per day for 20 years before quitting 15 years ago. On examination his temperature is 37oC (98.6oF), pulse is 75 beats/minute and regular, respirations are 15 breaths/minute, and blood pressure is 144/88 mm Hg. His lungs are clear to auscultation. On cardiac exam there is a loud, high-pitched grade III/IV blowing holosystolic murmur heard best at the apex with radiation to the axilla. Which of the following is the most likely diagnosis?

A) Aortic regurgitation

B) Aortic stenosis

C) Mitral regurgitation

D) Mitral stenosis

E) Mitral valve prolapse

Explanation:

The key piece of information in this vignette is the description of the murmur. This patient’s dyspnea and fatigue is likely from heart failure secondary to chronic mitral regurgitation (MR). The murmur of chronic mitral regurgitation is characterized as follows:

Quality

-    high-pitched, blowing

Location

-    usually best heard over the apex

-    usually with radiation to the axilla

Duration

-    classically holosystolic

Intensity

-    little correlation between intensity of murmur and severity of MR

-    intensity may be diminished in severe MR

Answer A: Aortic regurgitation is associated with a high-pitched, blowing, diastolic murmur and “water-hammer pulse” (bounding pulse with quick collapse).

Answer B: Aortic stenosis is associated with a systolic ejection click and a harsh, crescendo-decrescendo systolic murmur. Pulsus parvus et tardus can also be seen.

Answer D: Mitral stenosis is associated with an opening snap followed by a late diastolic murmur. The severity of the stenosis is inversely related to the timing between the snap and the start of the murmur.

Answer E: The murmur of mitral valve prolapse is a described as a mid-systolic click followed by a late systolic murmur and a loud S2.

Bottom Line: Mitral regurgitation is characterized by a high-pitched, blowing, holosystolic murmur heard best at the apex with radiation to the axilla.

Insight: Know heart murmurs like the back of your hand. This will allow you to work through clinical vignettes quickly and save time on the exam.

For more information, see http://emedicine.medscape.com/article/155618-overview

Question 3: A 72-year-old man presents to the physician’s office for three episodes of syncope in the past four months. The syncopal episodes are not associated with postural changes or sudden movements of the head. He also admits to chest pain with exertion over the past few months. On examination, his heart rate is 88 beats/minute, respirations are 18 breaths/minute, and blood pressure is 140/88 mm Hg. His lungs are clear to auscultation. On cardiac examination, there is a click followed by a harsh, grade III/VI crescendo-decrescendo systolic murmur heard best at the right upper sternal border with radiation to the carotids bilaterally. The maximal apical impulse is displaced laterally on the chest wall. There are no diastolic murmurs. Extremities are cool, but capillary refill is less than 2 seconds. There is no cyanosis or edema. Which of the following is the most likely diagnosis?

A) Aortic regurgitation

B) Aortic stenosis

C) Mitral regurgitation

D) Mitral stenosis

E) Mitral valve prolapse

Explanation:

The patient in this vignette is suffering from aortic stenosis (AS) as evidenced by his complaints of syncope and angina in association with the murmur. Outflow obstruction from aortic stenosis leads to exertional chest pain. Syncopal episodes associated with AS are thought to be related to transient episodes of tachyarrhythmias (syncope at rest) or sudden reduction systemic resistance and inability to maintain mean arterial pressure with enough forward flow from the obstructed aortic valve.

The murmur of aortic stenosis is characterized as follows:

Quality

-    Harsh, crescendo-decrescendo

Location

-    best heard at the right upper sternal border

-    usually with radiation to one or both carotids

Duration

-    ranges from early-mid systolic to pansystolic

-    the duration of the murmur correlates with the severity of the stenosis

Intensity

-    intensity does not correlate with the severity, rather the timing of the peak and the duration correspond to severity

Severity

-    augmented upon squatting; reduced during Valsalva

Answer A: Aortic regurgitation is associated with a high-pitched, blowing, diastolic murmur and “water-hammer pulse” (bounding pulse with quick collapse).

Answer C: Mitral regurgitation is associated with a blowing, holosystolic murmur heard best at the apex with radiation to the axilla. It is not usually associated with angina or syncope.

Answer D: Mitral stenosis is associated with an opening snap followed by a late diastolic murmur. The severity of the stenosis is inversely related to the timing between the snap and the start of the murmur.

Answer E: Mitral valve prolapse is associated with a mid-systolic click followed by a late systolic murmur and a loud S2.

Bottom Line: Aortic stenosis is characterized by a systolic ejection click followed by a crescendo-decrescendo systolic murmur best heard at the right upper sternal border with radiation to the carotids.

Know heart murmurs like the back of your hand. This will allow you to work through clinical vignettes quickly and save time on the exam.