Week 6 Heart Murmurs and Dysrhythmias Flashcards

1
Q

A patient has a cardiac murmur that peaks in mid-systole and is best heard along the left sternal border. The provider determines that the murmur decreases in intensity when the patient changes from standing to squatting and increases in intensity with the Valsalva maneuver. Which will the provider suspect is causing this murmur?

A Aortic stenosis

B Hypertrophic cardiomyopathy

C Mitral valve prolapse

D Tricuspid regurgitation

A

B Hypertrophic cardiomyopathy

These findings occur with hypertrophic cardiomyopathy. With aortic stenosis, the murmur is a harsh crescendo-decrescendo heard best at the right sternal border that decreases in intensity with the Valsalva maneuver. With mitral valve prolapse, the murmur is heard in mid- to late systole, is heard best at the left lower sternal border, and may have a click that moves to later systole or disappear with the Valsalva maneuver. With tricuspid regurgitation, the murmur may occur at early, mid, or late systole, is heard at the left lower sternal border, and decreases with the Valsalva maneuver.

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2
Q

Which are factors that can cause a heart murmur? (Select all that apply.)

A Backward flow through a septal defect

B Backward flow into a normal vessel

C Forward flow into a dilated vessel

D High rates of flow through a normal valve

E Low rates of flow into a cardiac chamber

A

A Backward flow through a septal defect

C Forward flow into a dilated vessel

D High rates of flow through a normal valve

High rates of flow into either normal or abnormal vessels can cause murmurs. Backward flow into septal defects, regurgitant valves, or PDAs can cause murmurs. Forward flow into constricted or irregular valves or into a dilated vessel can cause murmur. Backward flow into a normal vessel and low flow rates are not responsible for murmurs.

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3
Q

A 75-year-old male presents to your office for a complete physical examination before prostate surgery. On examination, you notice a 3/6 harsh, mid-systolic ejection murmur heard best at the upper right sternal border and radiating to the neck. S1 and S2 are normal. An echocardiogram demonstrates mild aortic stenosis. Currently he is asymptomatic.

The indications for valve replacement surgery include:

A Grade 4/6 murmur

B Requirement for major, semi-elective surgery, such as prostatectomy

C Severe aortic stenosis without symptoms and normal LV function

D Severe aortic stenosis in a patient undergoing coronary bypass grafting

E All of the above

A

D Severe aortic stenosis in a patient undergoing coronary bypass grafting

As a general rule, aortic stenosis is repaired when it becomes symptomatic. Repair of asymptomatic, severe aortic stenosis is indicated in the following scenarios: undergoing CABG or other valve or aorta surgery, LVEF < 50%, hypotension in response to exercise, or high likelihood of rapid progression. “A” is incorrect because the loudness of the murmur does not always correlate with its functional significance. “B” is incorrect as well. As long as the lesion is not hemodynamically significant, the patient should tolerate prostate surgery. “C” is incorrect because surgery is not usually necessary even in severe valvular disease without symptoms as long as the left ventricular function is normal. Note that it is not uncommon that patients with severe aortic stenosis report that they are asymptomatic, but they have modified their activity to avoid symptoms which may have occurred gradually so that they don’t recognize the decline.

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4
Q

Two years later, a patient with mild aortic stenosis returns for a checkup and states that he believes he has been having symptoms from his aortic stenosis

All of the following can occur with symptomatic aortic stenosis except:

A Left-to-right intracardiac shunt

B Exertional dyspneaE

C Syncope

D Angina

E Lightheadedness

A

A Left-to-right intracardiac shunt

Intracardiac shunts don’t occur with aortic stenosis. If you got this one wrong, back to anatomy for you! An isolated, fixed valvular lesion as an adult cannot cause intracardiac shunting. Exertional dyspnea, lightheadedness (presyncope), syncope, and chest pain are common symptoms in severe aortic stenosis.

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5
Q

The patient with mild aortic stenosis wants to know how often he will need to have a repeat echocardiogram given that he has mild disease. Your answer is:

A Every 3 to 5 years

B Every year

C Every 6 months

D When he develops symptoms

E None of the above

A

A Every 3 to 5 years

Patients with mild aortic stenosis who are asymptomatic can be followed by echocardiogram every 3 to 5 years. Patients with severe disease should have yearly echocardiography to evaluate for left ventricular dysfunction.

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6
Q

The primary care pediatric nurse practitioner (PNP) is performing a sports physical on an adolescent whose history reveals mild aortic stenosis (AS). What will the nurse practitioner recommend?

A Avoidance of all sports to prevent sudden death

B Clearance for any sports since this is mild

C Evaluation by a cardiologist prior to participation

D Low-intensity sports, such as golf or bowling

A

C Evaluation by a cardiologist prior to participation

Children with mild AS may participate in any sport but must have annual cardiac evaluations. Children with severe AS should avoid sports to prevent sudden death. The PNP should not clear the child for sports without a cardiology evaluation. Low-intensity sports are recommended for children with moderate AS.

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7
Q

An adolescent female has a history of repaired tetralogy of Fallot (TOF). Which long-term complication is a concern for this patient?

A Aortic stenosis

B Chronic cyanosis

C Mitral valve prolapse

D Ventricular failure

A

C Mitral valve prolapse

Patients with repaired TOF, especially adolescent females, are at risk for mitral valve prolapse. Aortic aneurysm is a long-term risk for those with a history of left-sided lesions. Chronic cyanosis is a concern for lesions causing Eisenmenger syndrome or defects causing right ventricular outflow obstruction. Ventricular failure can occur with prolonged aortic or pulmonic valvar stenosis.

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8
Q

During a routine well child exam on a 5-year-old child, the primary care pediatric nurse practitioner auscultates a grade II/VI, harsh, late systolic ejection murmur at the upper left sternal border that transmits to both lung fields. The child has normal growth and development. What will the nurse practitioner suspect?

A Aortic stenosis (AS)

B Patent ductus arteriosus (PDA)

C Pulmonic stenosis

D Tricuspid atresia

A

C Pulmonic stenosis

Pulmonic stenosis may be asymptomatic with a murmur as described above. Aortic stenosis is characterized by a louder, harsh systolic crescendo-decrescendo murmur at the upper right sternal border with radiation to the neck, LLSB, and apex. PDA has a machinery-like murmur. Tricuspid atresia is characterized by cyanosis.

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9
Q

The primary care pediatric nurse practitioner auscultates a new, grade II, vibratory, mid-systolic murmur at the mid-sternal border in a 4-year-old child that is louder when the child is supine. What type of murmur is most likely?

A Pathologic murmur

B Pulmonary flow murmur

C Still’s murmur

D Venous hum

A

C Still’s murmur

A Still’s murmur is characterized by a vibratory or musical low-grade sound, along the sternal border, which is louder when the child is supine or during inspiration. It is usually heard in children between the ages of 2 and 6 years old. Pathologic murmurs are usually harsh, not vibratory. A pulmonary flow murmur has a soft, blowing sound and radiates to the lung fields. A venous hum has a soft, high-pitched swishing sound.

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10
Q

During a well child assessment, the primary care pediatric nurse practitioner (PNP) auscultates a harsh, blowing grade IV/VI murmur in a 6-month-old infant. What will the nurse practitioner do next?

A Get a complete blood count to rule out severe anemia

B Obtain an electrocardiogram to assess for arrhythmia

C Order a chest radiograph to evaluate for cardiomegaly

D Refer to a pediatric cardiologist for further evaluation

A

D Refer to a pediatric cardiologist for further evaluation

A harsh, blowing murmur is suspicious for pathology, so a cardiology referral is warranted. The cardiologist will determine which tests and procedures should be performed.

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11
Q

A 75-year-old female presents to your office complaining of episodic palpitations with episodes of lightheadedness that are not concurrent with the palpitations. You perform an electrocardiogram in your office. An ECG shows fixed PR interval with an alternatingly nonconducting P wave and resultant dropped beats.What rhythm does this represent?

A First-degree heart block

B Second-degree heart block type I (Wenckebach)

C Second-degree heart block, type II

D Third-degree heart block

E Atrial flutter with variable block

A

C Second-degree heart block, type II

Your patient’s ECG shows a second-degree heart block, type II (Mobitz II). This is characterized by a fixed PR interval with an intermittently nonconducting P wave and resultant dropped beats. “A” is incorrect. First-degree heart block is characterized by a prolonged PR interval without any blocked beats (meaning every QRS is preceded by a P wave conducted with a long PR interval). The upper limit of normal of the PR interval is 0.2 seconds (and we admit that this one is darn close, but Mobitz II is the issue here). A second-degree heart block, Mobitz type I (Wenckebach), is defined by a progressively prolonged PR interval ending with a non-conducted P wave and a dropped beat. A third-degree heart block is characterized by no consistent pattern between the P waves and the QRS complex. “E” is incorrect because, by definition, atrial flutter is represented by a rapid atrial rate. In this patient, the rate is slow.

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12
Q

A 62-year-old female presents to your office with a history of occasional palpitations that are of great concern to her. She notes that she feels a racing heart that lasts for a matter of seconds and occurs every seven days or so. However, when she has the symptoms, she will generally get four to five episodes during that day. She denies any chest pain, dyspnea, lightheadedness, or other associated symptoms. You order an event monitor and it shows that the patient is having nonsustained episodes of monomorphic ventricular tachycardia lasting four beats or less each. She is asymptomatic except for the palpitations. The best approach at this point is to:

A Start an antiarrhythmic such as quinidine or mexiletine to control the heart rhythm

B Refer the patient to a cardiologist for an electrophysiologic (EP) study to determine the best drug to control this rhythm

C Implant an automatic defibrillator to prevent sudden death

D Implant a pacemaker

E Check serum potassium, magnesium, TSH, glucose, CBC

A

E Check serum potassium, magnesium, TSH, glucose, CBC

The first step in determining the treatment of this patient is to make sure that there is not an underlying metabolic abnormality that could predispose to this rhythm abnormality.

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13
Q

A patient reports sustained, irregular heart palpitations. What is the most likely cause of these symptoms?

A Anemia

B Atrial fibrillation

C Extrasystole

D Paroxysmal attacks

A

B Atrial fibrillation

Atrial fibrillation causes palpitations that are irregular and tend to be sustained. Anemia will cause rapid palpitations that are regular. Extrasystole causes palpitations or an awareness of isolated extra beats with a pause. Paroxysmal attacks start and terminate abruptly and are usually rapid and regular.

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14
Q

A 22-year-old female presents to your office with a history of palpitations. You are able to capture the arrhythmia on the monitor in your office. The rhythm strip shows evidence of isolated premature atrial contractions (PACs). She is otherwise healthy and taking no medications, and there is no family history of heart disease. All of the following are salient points of the history with regard to PACs except:

A Aged cheese consumption

B Caffeine use

C Tobacco use

D Alcohol use

E COPD

A

A Aged cheese consumption

Aged cheese can cause problems in combination with monoamine oxidase inhibitors (MAOIs). In combination with an MAOI, aged cheese and other sources of tyramine can cause a hypertensive emergency. However, this patient is not taking any medications. All of the other conditions and drugs listed can cause PACs. While there are conflicting data about the strength of the association caffeine, it is clear that COPD, tobacco, and alcohol can all cause an increase in sympathetic tone, leading to PACs. Neurologic abnormalities (e.g., stroke) can also be associated with PACs, as can some drugs (e.g., theophylline).

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15
Q

A rhythm strip shows increasing longer PR interval before a non-conducted P wave. What is the rhythm?

A Second-degree heart block, type I

B Second-degree heart block, type II

C Second-degree heart block, type II

D Sinus rhythm with non-conducted PACs

A

A Second-degree heart block, type I

This is a Wenckebach block, also known as second-degree heart block type I or Mobitz type I AV block. Thre is the progressive prolongation of the PR interval before a non-conducted P wave on the rhythm strip

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16
Q

A patient is bothered by her PACs. She is rather aware of them and finds them disconcerting.

What is the best pharmacologic therapy to consider at this point?

A Sotalol

B Metoprolol

C Trasylol

D Amiodarone

E Mountain Dew

A

B Metoprolol

A beta-blocker may help to reduce this patient’s PACs. “A” is incorrect because, while sotalol can be used for both atrial and ventricular arrhythmias, it is proarrhythmic and can cause torsades de pointes. Thus, it should be initiated in the hospital with monitoring and reserved for those with severe arrhythmias. “C” is incorrect because Trasylol is the trade name for aprotinin, an enzyme that was used to reduce bleeding during surgical procedures. “D” is incorrect because, like sotalol, amiodarone is proarrhythmic, and its use should be limited to those with significant arrhythmias.

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17
Q

Which of the following statements is true of mitral regurgitation?

a. It may be noted as a holosystolic murmur.
b. It is caused by stiff, noncompliant leaflets that limit flow from the left atrium to the left ventricle.
c. It occurs only as the result of congenital malformation of the mitral valve, which inhibits the contact and closure of the cusps.
d. It results in a prolonged PR interval on electrocardiogram.

A

a. It may be noted as a holosystolic murmur.

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18
Q

Which of the following statements about aortic stenosis (AS) is true?

a. The disease is typically manifested during midlife.
b. Once symptoms appear, life expectancy without surgery is about 10 years.
c. Symptoms are bothersome right from the early course of the disease.
d. The cardinal symptoms include dyspnea, angina, and syncope

A

d. The cardinal symptoms include dyspnea, angina, and syncope

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19
Q

When teaching your patient about aortic stenosis, which of the following statements that they might make would require more teaching from you?

a. “I will need antibiotic prophylaxis to prevent endocarditis.”
b. “You told me I still need aggressive treatment of my hypertension.”
c. “I’ll continue the use of diuretics and nitrates that my previous doctor gave me.”
d. “I’ll have a yearly Doppler echocardiography to evaluate the progression of the valve lesion.”

A

c. “I’ll continue the use of diuretics and nitrates that my previous doctor gave me.”

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20
Q

Which statement about mitral valve prolapse (MVP) is true?

a. MVP occurs in about 10% of the population
b. MCP is usually detected in older adults.
c. The incidence is equal in men and women younger than age 20.
d. The incidence is more common in women younger than age 20

A

d. The incidence is more common in women younger than age 20

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21
Q

When indicated, which procedure needs endocarditis prophylaxis?

a. Vaginal or cesarean deliveries
b. Insertion or removal of intrauterine devices
c. Dental procedures or extractions
d. Body piercings

A

c. Dental procedures or extractions

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22
Q

Murmurs are graded according to their intensity (loudness). A murmur that is audible with the stethoscope off the chest is a

a. Grade III
b. Grade IV
c. Grade V
d. Grade VI

A

d. Grade VI

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23
Q

An asymptomatic 75-year-old Asian woman presents to primary care clinic for her health maintenance exam. Her pulse is irregular in pattern and amplitude. Her electrocardiogram (ECG) shows: no discernable p waves

Describe what your diagnosis is and your findings on the EKG? If a patient becomes symptomatic, what would the symptoms be?

A

This patient has atrial fibrillation (AF), the most common arrhythmia. Atrial fibrillation is a supraventricular arrhythmia caused by uncoordinated electrical activity in the atria. It results in an irregular ventricular response that can lead to hemodynamic instability

Atrial fibrillation is typically diagnosed by an irregular R-R interval and absence of P waves on electrocardiogram (ECG). Other common characteristics include fibrillatory (F) waves and a narrow QRS complex.

Fibrillatory waves are most likely to be seen in lead V1. Atrial fibrillation must be distinguished from other rhythms that are irregularly irregular, such as multifocal atrial tachycardia and atrial flutter with varying atrioventricular (AV) block

This patient is asymptomatic, which is a common presentation of AF. Patients who present with symptoms often describe fatigue, palpitations, weakness, dizziness, and reduced exercise tolerance.2,3

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24
Q

Types of a fib

A

Paroxysmal – less than 7 days and self-terminates

Persistent – greater than or equal to 7 days or resolves with cardioversion after 48 hours

Permanent – no further efforts are being pursued to restore sinus rhythm

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25
Q

What are the major risks associated with atrial fibrillation?

A

stroke and other thromboembolic events

The Framingham Study found nearly a 5-fold risk of stroke in patients with atrial fibrillation compared to patients without AF. Atrial fibrillation is estimated to cause 15% of all strokes. Strokes caused by AF are also more severe than non-AF-related strokes.

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26
Q

What causes atrial fibrillation?

A

most common causes of AF are structural abnormalities that result from hypertension, coronary artery disease, valvular heart disease, cardiomyopathies, and heart failure

These processes cause increased left atrial pressure, causing atrial dilation and wall stress. They may also cause fibrosis of myocardial tissue, which can disturb the generation and propulsion of atrial conduction. Sleep apnea, obesity, alcohol, drugs, and hyperthyroidism can promote AF by altering atrial cell structure and/or function.

The ATRIA trial showed that the prevalence of atrial fibrillation increases dramatically with age, with 9% of patients 80 years and older found to have this condition compared to only 0.1% of patients younger than 55 years old.

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27
Q

workup for afib

A

● CBC, creatinine, UA, and a test for diabetes mellitus (baseline tests)
● TSH and free T4 (FT4) (to rule out hyperthyroidism)
● Urine toxicology and alcohol screen (to rule out drug-induced arrhythmia)
● Transthoracic echocardiogram (to rule out structural heart disease and investigate the possibility of preexisting cardiac thrombi)
A predisposing or associated condition exists in 80% to 90% of cases.

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28
Q

The increased risk of stroke associated with atrial fibrillation is due to which of the following etiologies?

A. Blood pooling in the atrial appendage

B. Shearing of red blood cells

C. Hypercoagulability

D. Hypertension

A

A. Blood pooling in the atrial appendage

As the atria fibrillate, blood pools in the atrium. The blood sometimes collects itself into a clot in the atrial appendage, which can embolize to the brain, leading to stroke. Shearing of red blood cells is a phenomenon seen especially in valvular heart disease; it is not the mechanism of stroke in atrial fibrillation (AF). Patients with atrial fibrillation do not function in a hypercoagulable state. While AF and hypertension share many of the same risk factors, the increased risk of stroke as a result of atrial fibrillation is due to blood pooling in the atria.

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29
Q

Which of the following forms of AF carries the highest rate of stroke?

A. Paroxysmal atrial fibrillation

B. Permanent atrial fibrillation

C. Neither paroxysmal nor permanent atrial fibrillation carries a high risk of stroke.

D. Paroxysmal and permanent atrial fibrillation carry the same risk of stroke.

A

D. Paroxysmal and permanent atrial fibrillation carry the same risk of stroke.

Atrial fibrillation (AF) is associated with a 5-fold increased risk of stroke. Paroxysmal atrial fibrillation is episodic and resolves spontaneously. Permanent atrial fibrillation refers to AF that has persisted, often despite attempts to restore sinus rhythm. Paroxysmal and permanent AF carry the same risk of stroke.

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30
Q

Which of the following medications should be used as first-line therapy for rate control in patients with AF?

A. Digoxin

B. Beta blockers

C. Amiodarone

D. Angiotensin-converting enzyme (ACE) inhibitors

A

B. Beta blockers

Beta blockers (metoprolol, atenolol) and non-dihydropyridine calcium channel blockers (diltiazem, verapamil) are first-line therapy for rate control in patients with atrial fibrillation (AF). Digoxin should not be used as first-line therapy or monotherapy for rate control, but has been used as an adjunct to beta blockers and calcium channel blockers to increase parasympathetic tone. Amiodarone may be used for rate control in patients with AF, but because of its delayed action and potential toxicity, amiodarone is used when beta blockers or calcium channel blockers are ineffective or insufficient to achieve rate control. Current data do not support the use of ACE inhibitors to prevent cardiovascular events in AF, though researchers have proposed that through reduction in atrial stretch, they may be helpful in preventing adverse outcomes in patients with AF.

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31
Q

WHAT ARE RED FLAG SYMPTOMS OF A HEART MURMUR?

A
holosystolic 
diastolic 
>/= grade 3
increasing intensity when standing
associated w/ new extra heart sound
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32
Q

A 10 MONTH OLD PATIENT PRESENT TO THE CLINIC FOR A POTENTIAL EAR INFECTION. DURING EXAM, THE PROVIDER NOTES A NEW ONSET SHORT, MUSICAL, SYSTOLIC MURMUR. WHAT SHOULD THE PROVIDER DO NEXT?

A

URGENT REFERRAL TO CARDIOLOGY (ANY CHILD < 1 YEAR OLD SHOULD BE REFERRED, EVEN IF THE MURMUR APPEARS INNOCENT)

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33
Q

YOUR PATIENT PRESENTS WITH A HARSH, HOLOSYSTOLIC, MURMUR THAT IS BEST HEARD AT THE APEX AND RADIATES TO THE AXILLA. THIS IS MOST LIKELY WHAT?

A

MITRAL REGURGITATION

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34
Q

HOW OFTEN SHOULD PATIENTS WITH MITRAL VALVE PROLAPSE SHOULD GET AN ECHOCARDIOGRAM?

A

Q 3-5 YEARS

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35
Q

DESCRIBE THE CLASSIC MURMUR FOUND IN HYPERTROPHIC CARDIOMYOPATHY?

A

PANSYSTOLIC MURMUR, QUIETER WITH SQUATTING/LOUDER WHEN STANDING

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36
Q

systolic murmurs

A

MR PM AS MVP = Mr. Payton Manning as MVP

mitral regurgitation (MR)
physiologic murmur (tricuspid regurg) (PM)
aortic stenosis (AS)
mitral valve prolapse (MVP)

murmurs heard WITH pulse

pulmonic stenosis
VSD

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37
Q

diastolic murmurs

A

ARMS PaRTS

aortic regurgitation (AR)
mitral stenosis (MS)
pulmonary regurgitation (PR)
tricuspid stenosis (TS)

ALWAYS bad, not heard in conjunction with pulse

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38
Q

aortic stenosis presentation

A

harsh systolic crescendo-decresendo murmur WITH ejection click

louder with squatting
quiet w/ valsalva/standing

upper right sternal border 2nd intercostal, radiates to carotid

split s2, s4, narrow pulse pressure

SAD = syncope, angina, dyspnea

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39
Q

mitral regurgitation presentation

A

holoSYSTOLIC murmur

apex, radiates to axilla area

diminished S1, wide S2, S3 gallop

asymptomatic, then signs of HF as progresses:

  • fatigue
  • exertional dyspnea
  • orthopnea
  • palpitations
  • R-sided HF
  • acute pulmonary edema
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40
Q

mitral valve prolapse presentation

A

midSYSTOLIC click, honking

apex, LLSB

standing increases murmur, squatting decreases

asymptomatic
palpitations, chest discomfort, syncope

common women 15- 30 y.o.

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41
Q

tricuspid regurgitation presentation

A

holoSYSTOLIC, blowing murmur

LLSB, radiates to right sternal border

increased with inspiration, decreased with expiration

asymptomatic
fatigue, exertional dyspnea
severe decreased CO
sustained pericordial lift

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42
Q

aortic regurgitation presentation

A

early decrescendo diastolic murmur
loud, blowing, high pitched

LLSB, Erb’s point

heard loudest when leaning forward post exhale

widened pulse pressure

palpitations, head pounding, angina, orthopnea/dyspnea, fatigue

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43
Q

mitral stenosis presentation

A

low-pitched DIASTOLIC rumble, opening SNAP, loud S1

apex, heard best in left lateral recumbent position

dyspnea, cough, sudden change in heart rhythm & volume status
orthopnea, PND, hemoptysis
thrombosis, emboli possible

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44
Q

tricuspid stenosis presentation

A

diastolic rumble, decrescendo, low-pitched, ejection click

4th or 5th LLSB, near xiphoid process
increases w/ inspiration

pulmonary congestion, fatigue, R-sided HF symptoms - hepatomegaly ascites, edema

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45
Q

pulmonic regurgitation presentation

A

decrescendo DIASTOLIC
graham-steele murmur

LUSB: 3rd- 4th L intercostal space

increased when sitting/leaning forward & during inspiration

asymptomatic
can lead to R-sided HF: JVD, RV enlargement

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46
Q

pulmonic stenosis presentation

A

SYSTOLIC crescendo-decrescendo murmur
ejection click, S2 wide split
harsh, medium pitch

left 2-3 intercostal space; if loud radiates to left shoulder, neck

increased with valsalva

asymptomatic mild- mod dx
severe - dyspnea & fatigue

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47
Q

benign or innocent murmur presentation

Still murmur

A

early SYSTOLIC, crescendo-decrescendo

musical or vibratory quality

mid-left sternal border and apex

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48
Q

grade 1 murmur

A

very faint

heard with intent listening, may not be heard in all positions

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49
Q

grade 2 murmur

A

quiet, but heard immediately after placing stethoscope on chest

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50
Q

grade 3 murmur

A

moderately loud

51
Q

grade 4 murmur

A

loud, with palpable thrill

52
Q

grade 5 murmur

A

very loud with thrill

may be heard with stethoscope partly off chest

53
Q

grade 6 murmur

A

very loud with thrill

may be heard with stethoscope entirely off chest

54
Q

aortic stenosis management

A

EKG, ECHO, consider CXR
depending on severity refer cardiac cath

asymptomatic: monitor

mod- severe: NO competitive sports, tx HTN & HLD
refer out to valvular heart center

stage B or higher: surgical intervention (AVR or TAVR)

55
Q

stage A VHD

A

at risk

pts with RF for development of VHD

56
Q

Stage B VHD

A

progressive

progressive VHD (mild to mod severity and asymptomatic)

57
Q

Stage C VHD

A

asymptomatic severe

asymptomatic patients who have criteria for sever VHD:

  • C1: asymptomatic w/ severe VHD in whom L or R ventricle remains compensated
  • C2: asymptomatic w/ severe VHD, w/ decompensation of L or R ventricle
58
Q

Stage D VHD

A

symptomatic severe

developed symptoms as result of VHD

59
Q

mitral regurgitation management

A

EKG (afib common), ECHO, consider CXR
consider cardiac cath

asymptomatic, NSR, and no LV enlargement no exercise restrictions
symptomatic: NO competitive sports

tx comorbid afib antiarrhythmias or anticoags
BB, ACE-I, aldosterone antagonists

repair valve

60
Q

mitral valve prolapse management

A

EKG, ECHO, TTE, TEE

monitor ECHO every 3-5 years

asymptomatic: monitor

BB to manage PVCs or SVT
ASA/anticoag for afib

surgery for severe prolapse

61
Q

tricuspid regurgitation management

A

EKG, ECHO

depends on underlying causes, presenting symptoms, and severity

valve replacement

diuretics, aldosterone antagonist, BB if indicated (signs of HF)

62
Q

pulmonic stenosis management

A

TTE, EKG

balloon valvuloplasty
valve replacement if symptmatic

63
Q

aortic regurgitation management

A

EKG, TTE, ECHO, CXR

refer cardio (diastolic murmur)

asymptomatic: annual f/u

surgical intervention for Stage C or D
replacement when EF < 55%

tx HTN: dihydropine CCB, ACE-I/ARBs
tx afib/bradycardia

64
Q

pulmonic regurgitation management

A

ECHO

valve replacement if symptomatic

65
Q

mitral stenosis mangement

A

TEE (RV hypertrophy), EKG (afib), CXR (enlarged L atrium)

refer cardio (diastolic murmur)

afib - anticoags
infectious endocarditis prophylaxis

valve center - valvotomy or replacement

66
Q

tricuspid stenosis management

A

EKG, ECHO

refer cardio (diastolic murmur)

salt restriction, bedrest, diuretics r/t R sided HF
BB

surgical tx: repair/replace valve

67
Q

acyanotic murmurs

A

no issues with deoxygenated blood mixing with oxygenated blood and being pumped into systemic system

left to right shunts

VSD
PDA
ASD
Coarctation of aorta
aortic stenosis 
pulmonary stenosis
68
Q

cyanotic murmurs

A

deoxygenated blood is moving to L side and being pumped into systemic circulation

right to left shunt

tetralogy of fallot
transposition of great arteries 
truncus arteriosus 
Tricuspid atresia
pulmonary atresia 
hypoplastic left heart syndrome
69
Q

congenital heart disease (CHD) cause

A

developmental alteration in or failure of embryonic heart to progress beyond early developmental stage

occurs in 2nd to 8th weeks of gestation d/t:

  • genetics
  • environmental factors
  • multifactoral influences
  • most have no identifiable causes
70
Q

CHD general clinical presentation

A
abnormal growth or VS
- tachypneic after feeding 
adventitious breath sounds 
chest contour, dysmorphic features
GI findings
CV findings - when auscultating listen when standing, sitting, lying, and left lateral position
71
Q

ventricular septal defect (VSD)

A

defect between septum of ventricle
higher pressure on L side, blood from L side of ventricle will be shunted across from L to R into RV

most common type

loud, harsh blowing holosystolic murmur (LLSB)

increases with Valsalva

72
Q

Atrial septal defect (ASD)

A

hole between septum of atrium
oxygenated blood moves back into R side of heart w/ deoxygenated blood - pulmonary artery - lungs - reoxygenated

relatively common, more common in females

mid-systolic murmur, widened S2 split

73
Q

patent ductus arteriosus (PDA)

A

PDA fails to close, saturated blood moves from aorta into pulmonary artery

PDA should close at 24-72 hours old

harsh, machine like murmur; L clavicle L 2nd space

74
Q

coarctation of aorta

A

part of aorta is constricted
aorta gets squeezed down, obstructs blood flow - increases afterload - blood supply decreased to abd organs and lower periphery bc of decrease in blood flow

difference in BP in arms and legs
pulses stronger in upper extremity vs lower extremities

short systolic murmur 3rd and 4th intercostal spaces 
radial- femoral delay 
BP arms > legs
cyanosis
tachypnea 
signs of HF
75
Q

tetralogy of fallot

A
  1. ventricular septal defect
  2. R ventricular outflow tract obstruction
  3. overriding aorta (aorta arises from RV instead of LV)
  4. RV hypertrophy

must be ID’ed right away, requires surgical repair ASAP

“tet spells” cyanotic
poor feeding, FTT
clubbing
exertional dyspnea

harsh holosystolic murmur LUSB
RV heave

76
Q

transposition of great arteries

A

aorta arises from RV, pulmonary artery from LV
aorta and pulmonary artery flipped

NOT compatiable with life, need PFO or PDA to survive

possible split S2, 2nd heart sounds LOUD

cyanosis, tachypnea, acidosis

77
Q

tricuspid atresia

A

blind pouch at tricuspid valve

tricuspid valve not developed

desaturated blood enters R atrium, not where to go, shunts from R to L via PFO to get to L side of heart bypasses pulmonary artery and lungs

recognize and surgically repair ASAP

cyanosis, grade I-II/IV systolic murmur, hepatomegaly

78
Q

pulmonary atresia

A

failure of pulmonary valve to develop, blind pouch

high ventricular pressure in R side of heart

associated with underdeveloped tricuspid valve

79
Q

truncus arteriosus

A

failure of common great vessels to divide
One big wide opening
pulmonary and aorta mixed together

decreased O2 sat

must be ID’d and tx ASAP

ejection click, loud single 2nd heart sound
mid diastolic mitral flow murmur @ apex

increased pulse pressure
peripheral pulses accentuated & bounding

80
Q

hypoplastic left heart syndrome (HLHS)

A

uncommon

LV severely underdeveloped

only RV works

more in M than F

NOT compatible with life, most die within 1st few months if untreated

5 year survival rates low

should be ID’ed before DC from hospital

loud single 2nd heart sound
typically no murmur

81
Q

CHD management

A

Identify and refer immediately to pedi cardiology

correct underlying problem
oxygen - caution in L to R shunt (acyanotic)

two consequences: HF or death

82
Q

management of “tet” spells

A
knee-chest position 
oxygen therapy 
IV fluid bolus 
morphine 
IV BB
IV pheynylephrine
83
Q

Afib causes/RF

A
idiopathic 
HTN
valvular heart dx
hypothyroidism 
CAD
cardiomyopathies 
HF
OSA
obesity
alcohol
drugs
84
Q

afib presentation

A

asymptomatic

fatigue, palpitations, weakness, dizziness, reduced exercise tolerance

85
Q

afib diagnostics

A

EKG demonstrating irregular R-R intervals, no distinct P waves, and atrial cycle length < 200 ms
ECHO
CBC, Cr, UA/drug screen/ETOH, A1c, glucose, TSH, free t4

86
Q

afib management

A

rate control:
BB (metoprolol) or non-dihydropyridine CCB ok to start if rate controlled
uncontrolled rate = cardio referral

reduce clotting:
anticoagulation, calculate CHADS-VASC 2 score

refer cardiology for TEE, cardioversion

if new onset, cardiovert

continues w/ issues ablation

87
Q

CHADS VAS score

A

evaluates stroke risk

CHF (1)
HTN (1)
Age > 75 (2)
DM (1)
Stroke/thromboembolism hx (2)
Vascular dx (1)
Age 65- 74 (1) 
Sex - female (1)
88
Q

CHADS VAS score risk

A

low risk = 0
- no anticoagulation, full dose ASA only

Low- moderate risk = 1
- either anticoagulation or full dose ASA

moderate-high risk = 2+
- anticoagulation recommended

Warfarin gold standard, narrow therapeutic index

89
Q

cardioversion

A

electric or pharmacologic

for new onset and symptomatic a fib (angina, dyspnea, hemodynamic instability)

risk of thromboembolic event in first few days after cardioversion

anticoag prior to, during, and after procedure preferred
UNLESS TEE confirms no thrombus at time of cardioversion, no anticoags needed

90
Q

urgent cardioversion anticoags

A

heparin, then warfarin for 4 weeks

91
Q

non-urgent cardioversion anticoags

A

start warfarin 3 weeks prior and continue for 4 weeks

92
Q

young pts and afib

A

attempt to restore to NSR to prevent remodeling and symptoms at night

93
Q

PCP role in afib

A

ID afib, determine risk of stroke, initiate anticoags
Get an ECHO!
Consider antiarrhythmic meds

94
Q

Paroxysmal afib

A

Occurs for < 7 days & self terminates

95
Q

Persistent afib

A

> 7 days or resolved w/ cardioversion after 48 hrs

96
Q

Permanent afib

A

No further efforts are being pursued to restore NSR

97
Q

atrial flutter

A

Sawtooth pattern!! 4 flutters to 1 QRS conduction

Results from an abnormality of conduction in the atrium
Ventricles working normally

98
Q

Supraventricular Tachycardia (SVT)

A

Impulses above the ventricles in the atria, over 150 bpm
Proximal, self limiting, too fast to differentiate underlying rhythm
P & T wave continuous
Can be slowed w/ adenosine in the ER
If outpt, try vagal maneuvers to slow it down
If not successful → ER!!!

99
Q

Q waves on EKG

A

pathologic

suggestive of prior myocardial injury

100
Q

pacemaker needed in

A

second degree AV block type 2

third degree AV block

101
Q

1st degree AV block

A

P wave before every QRS BUT delayed conduction through AV node

PR segment > 0.20 sec

generally asymptomatic

observe, no further tx

increased risk afib

102
Q

2nd degree AV block type 1

A

Movitz 1 aka winkebach

progressive prolongation of PR interval, eventually P wave drops off - longer, longer, drop

asymptomatic

benign rhythm, but monitor

if d/t med STOP (BB, CCB)

103
Q

2nd degree AV block type 2

A

Movits 2

may not see P wave w/ every QRS
intermittent non-conducted P wave w/o warning

PR interval constant

HIGH RISK of complete heart block & asystole

REFER FOR PACEMAKER

104
Q

causes of 2nd degree AV block type 2

A
anterior MI
septal infarct
fibrosis
autoimmune - lupus 
myocarditis 
lyme dx
meds
electrolyte imbalances
105
Q

3rd degree AV block

A

complete absence of AV node conduction
P waves NEVER r/t QRS, disassociation between them

HIGH RISK asystole, Vtach, DEATH

NEEDS PACEMAKER

106
Q

3rd degree AV block causes

A

post MI

meds: BB, CCB, adenosine, amiodarone

107
Q

Wolf Parkinson white Syndrome

A

notch in QRS = delta wave

REFER cardio - ablation

rapid fluttering HR
dizziness, lightheadedness, SOB, fatigue, anxiety, chest pain, dyspnea

infants: cyanosis, poor feeding, rapid breathing, restlessness

108
Q

v tach

A

tachycardia originates in ventricles
wide QRS segment > 0.12 sec

more than 3 PVCs in a row
rate > 100 bpm

dizziness, lightheadedness, chest pain, neck tightness, SOB, syncope

109
Q

antiarrythmic agents

A

typically needs stress test or echo prior to tx

goal restore rhythm and conduction, prevent more serious dysrhythmias

Class I: sodium channel blockers (flecanide)
Class II: BB (metoprolol)
Class III: potassium channel blockers (Sotalol)
Class IV: CCB (verapamil)

amiodarone = most effective anti-arrhythmia, affects across ALL classes

110
Q

An 80 year old F has a systolic murmur that is best heard at the apex of the heart. What murmur is likely?

A. mitral stenosis

B. aortic stenosis

C. mitral regurgitation

D. aortic regurgitation

A

C. mitral regurgitation

heard at apex (mitral point), systolic murmur

111
Q

Which patient is most likely to exhibit a physiologic murmur and why?

A. 70 y.o. w/ HF

B. 45 y.o. w/ HTN

C. 30 y.o. marathon runner

D. 15 y.o.

A

D. 15 y.o.

heart is growing and stretching

112
Q

A 55 y.o. c/o sternal discomfort when walking and presents with a soft murmur near the 2nd intercostal space to the right sternum. Is is audible during systole.

Is this a significant murmur?

What is it?

A

Yes, significant is the chest pain angina?

murmur is most likely aortic stenosis

113
Q

A 67 y.o. has been diagnosed w/ mitral stenosis. What do you expect when listening to the murmur?

A. late systolic click near apex

B. radiation of soft diastolic sounds into neck and carotid arteries

C. diastolic sounds heard loudest near apex

D. soft diastolic sounds in left mid-clavicular area

A

C. diastolic sounds heard loudest near apex

114
Q

A 43 y.o. M has an audible diastolic murmur best heard in the mitral listening point. There is no audible click. His status has been monitored for the past 2 years. This murmur is probably:

A. Mitral valve prolapse

B. Acute mitral regurgitation

C. Chronic mitral regurgitation

D. mitral stenosis

A

D. mitral stenosis

MVP is unlikely since MVP is a systolic murmur, no audible click, and MVP has late-to-mid systolic click.
MR usually develops after rupture of chordae tendinea, ruptured papillary muscle after MI, or secondary to bacterial endocarditis. Symptoms of failure would appear with abrupt clinical deterioration in patient. A 2 year course for this patient as described would not be appropriate if this were an acute development. Dilation o the left atrium and ventricle is typical in chronic MR since both chambers are affected from regurgitant blood flow across the diseases valve, but MR is a systolic murmur, not a diastolic.

This is MS, as MS produces the only diastolic murmur listed in the question.

115
Q

A 75 y.o. pt who has aortic stenosis wants to know what symptoms indicate worsening of his stenosis. you reply:

A. palpitations and weakness

B. ventricular arrhythmias

C. SOB and syncope

D. fatigue and exercise intolerance

A

C. SOB & syncope

the 3 most common symptoms of aortic stenosis are angina, syncope, and heart failure as evidenced by dyspnea. Syncope is usually exertional. Angina may be d/t aortic stenosis, but underlying coronary artery disease usually accounts for half of anginal symptoms in these patients. There is usually a prolonged asymptomatic phase, but the presence of symptoms usually indicated a need for valve replacement. Without replacement, there is a rapid decline in the patient’s status and death will ensue

116
Q

Which choice best characterizes a patient who has aortic regurgitation?

A. Long asymptomatic period followed by exercise intolerance, then dyspnea at rest

B. An acute onset of SOB in the 5th or 6th decade

C. Dyspnea on exertion for a long period of time before sudden cardiac death

D. A long asymptomatic period with sudden death, usually during exercise

A

A. Long asymptomatic period followed by exercise intolerance, then dyspnea at rest

The natural course of AR is that the patient has a long asymptomatic period with slowing of activities but remains essentially asymptomatic. SOB develops with activity and finally SOB at rest. The LV eventually fails unless the aortic valve is replaced

117
Q

The valve most commonly involved in chronic rheumatic heart dx

A. aortic

B. mitral

C. pulmonic

D. tricuspid

A

B. mitral

The mitral valve has a propensity for disorders secondary to rheumatic heart dx. Rarely is the pulmonic valve involved, but the aortic and tricuspid valves follow in descending order of involvement. Following an episode of rheumatic fever, which occurs infrequently in the U.S. today but is common in developing countries, the valves can become stenotic or regurgitant. This is a major cause of valvular heart dx in the U.S. and is seen primarily in immigrants.

118
Q

A 28 y.o. has a grade 2 murmur. Which characteristic indicates a need for referral?

A. A fixed split

B. An increase in splitting with inspiration

C. A split S2 with inspiration

D. Changes in laterality with position change

A

A. A fixed split

A split is created because of closure of valves. For example, an S2 is created by closure of the aortic and pulmonic valves. Normally these split with inspiration and almost never with expiration. Splits should never be fixed. This indicates pathology such as an atrial septal defect, pulmonic stenosis, or possibly mitral regurgitation. In any event, the patient needs initial eval and echocardiogram because fixed splits are always considered abnormal. He will be referred to cardiology.

119
Q

The usual course of mitral valve prolapse:

A. Is benign

B. Results in sudden cardiac death

C. Results in chronic heart failure

D. Is associated with multiple episodes of emboli

A

A. Is benign

The usual course of MVP is benign and most patients with MVP are asymptomatic. A murmur may be present and is best auscultated with the diaphragm of the stethoscope over the cardiac apex. In a minority of patients symptoms of HF or sudden death may occur. When HF results, it is usually as a result of MR. Embolization may occur, but this is not common or usual in the majority of patients.

120
Q

A patient who has MVP reports chest pain and frequent arrhythmias. In the absence of other underlying cardiac anomalies, the drug of choice to treat the s/s is:

A. Lisinopril

B. Metoprolol

C. Amlodipine

D. Chlorthalidone

A

B. Metoprolol

BB’s like metoprolol are indicated to alleviate atrial or ventricular arrhythmias associated with MVP. However, long-term effectiveness of BB is uncertain. Most patients with MVP who do not have symptoms of arrhythmias or ectopy at rest usually do not require further evaluation. however they should be monitored at least annually for a change in their condition.

121
Q

Where would the murmur associated with mitral regurgitation best be auscultated?

A. aortic listening point

B. mitral listening point

C. pulmonic listening point

D. tricuspid listening point

A

B. mitral listening point

The mitral listening point is where the murmur associated with MR can be heard loudest. Murmurs tend to be loudest at the point where they originate. In this case, that is the mitral listening point. As the LV enlarges secondary to MR, the apical impulse becomes displaced left and laterally and becomes diffuse.

122
Q

The diagnosis of mitral valve prolapse can be confirmed by:

A. CXR

B. Echo

C. EKG

D. physical exam

A

B. ECHO

The best means to diagnose MVP is with an ECHO. It will identify bulging of either or both of the leaflets into the left atrium. Approximentaly 2% of the US population has MVP. A CXR will not enable visualization of the leaflets. EKG identifies the heart’s electrical activity. A physical exam may provide great clues to MVP, but in the absence of definitive mid to late systolic clicks, a diagnosis cannot be confirmed.

123
Q

A patient with MR has developed the most common arrhythmia associated with MR. The intervention most likely to prevent complications from this arrhythmia is:

A. Valve replacement

B. BB administration

C. Anticoagulation

D. Immediate referral for a pacemaker

A

C. anticoagulation

The most common arrhythmia associated with MR is atrial fibrillation. Anticoagulation with warfarin will help prevent arterial embolism that can result in stroke or MI. A fib occurs because the fibers in the atrium are stretched as the atrium dilates. The stretch results in conduction defects, notably, atrial fibrillation.

124
Q

A patient with aortic stenosis has been asymptomatic for decades. On routine exam he states that he has had some dizziness associated with activity but no chest pain or SOB. The best course of action is:

A. Assess carotid arteries for bruits

B. Order a CBC, metabolic panel, and UA

C. Refer to cardiology

D. Monitor closely for worsening oh his status

A

C. Refer to cardiology

In a pt with AS who has been asymptomatic for decades, one should be alert for symptoms that will precede angina, HF, and syncope. Dizziness precedes syncope in these patients and so this is an early indication that the patient is becoming symptomatic form his AS. Once symptoms develop it is a rapid downhill course. Dizziness, CP, or exercise intolerance are important symptoms to assess in a previously asymptomatic patients with AS. This patient needs a referral to cardiology.