Week 6 Heart Murmurs and Dysrhythmias Flashcards
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
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.
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 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.
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
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.
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 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.
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 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.
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
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.
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
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.
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
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.
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
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.
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
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.
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
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.
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
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.
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
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.
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 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).
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 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
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
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.
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. It may be noted as a holosystolic murmur.
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
d. The cardinal symptoms include dyspnea, angina, and syncope
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.”
c. “I’ll continue the use of diuretics and nitrates that my previous doctor gave me.”
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
d. The incidence is more common in women younger than age 20
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
c. Dental procedures or extractions
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
d. Grade VI
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?
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
Types of a fib
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
What are the major risks associated with atrial fibrillation?
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.
What causes atrial fibrillation?
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.
workup for afib
● 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.
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. 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.
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.
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.
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
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.
WHAT ARE RED FLAG SYMPTOMS OF A HEART MURMUR?
holosystolic diastolic >/= grade 3 increasing intensity when standing associated w/ new extra heart sound
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?
URGENT REFERRAL TO CARDIOLOGY (ANY CHILD < 1 YEAR OLD SHOULD BE REFERRED, EVEN IF THE MURMUR APPEARS INNOCENT)
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?
MITRAL REGURGITATION
HOW OFTEN SHOULD PATIENTS WITH MITRAL VALVE PROLAPSE SHOULD GET AN ECHOCARDIOGRAM?
Q 3-5 YEARS
DESCRIBE THE CLASSIC MURMUR FOUND IN HYPERTROPHIC CARDIOMYOPATHY?
PANSYSTOLIC MURMUR, QUIETER WITH SQUATTING/LOUDER WHEN STANDING
systolic murmurs
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
diastolic murmurs
ARMS PaRTS
aortic regurgitation (AR) mitral stenosis (MS)
pulmonary regurgitation (PR) tricuspid stenosis (TS)
ALWAYS bad, not heard in conjunction with pulse
aortic stenosis presentation
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
mitral regurgitation presentation
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
mitral valve prolapse presentation
midSYSTOLIC click, honking
apex, LLSB
standing increases murmur, squatting decreases
asymptomatic
palpitations, chest discomfort, syncope
common women 15- 30 y.o.
tricuspid regurgitation presentation
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
aortic regurgitation presentation
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
mitral stenosis presentation
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
tricuspid stenosis presentation
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
pulmonic regurgitation presentation
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
pulmonic stenosis presentation
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
benign or innocent murmur presentation
Still murmur
early SYSTOLIC, crescendo-decrescendo
musical or vibratory quality
mid-left sternal border and apex
grade 1 murmur
very faint
heard with intent listening, may not be heard in all positions
grade 2 murmur
quiet, but heard immediately after placing stethoscope on chest
grade 3 murmur
moderately loud
grade 4 murmur
loud, with palpable thrill
grade 5 murmur
very loud with thrill
may be heard with stethoscope partly off chest
grade 6 murmur
very loud with thrill
may be heard with stethoscope entirely off chest
aortic stenosis management
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)
stage A VHD
at risk
pts with RF for development of VHD
Stage B VHD
progressive
progressive VHD (mild to mod severity and asymptomatic)
Stage C VHD
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
Stage D VHD
symptomatic severe
developed symptoms as result of VHD
mitral regurgitation management
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
mitral valve prolapse management
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
tricuspid regurgitation management
EKG, ECHO
depends on underlying causes, presenting symptoms, and severity
valve replacement
diuretics, aldosterone antagonist, BB if indicated (signs of HF)
pulmonic stenosis management
TTE, EKG
balloon valvuloplasty
valve replacement if symptmatic
aortic regurgitation management
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
pulmonic regurgitation management
ECHO
valve replacement if symptomatic
mitral stenosis mangement
TEE (RV hypertrophy), EKG (afib), CXR (enlarged L atrium)
refer cardio (diastolic murmur)
afib - anticoags
infectious endocarditis prophylaxis
valve center - valvotomy or replacement
tricuspid stenosis management
EKG, ECHO
refer cardio (diastolic murmur)
salt restriction, bedrest, diuretics r/t R sided HF
BB
surgical tx: repair/replace valve
acyanotic murmurs
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
cyanotic murmurs
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
congenital heart disease (CHD) cause
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
CHD general clinical presentation
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
ventricular septal defect (VSD)
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
Atrial septal defect (ASD)
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
patent ductus arteriosus (PDA)
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
coarctation of aorta
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
tetralogy of fallot
- ventricular septal defect
- R ventricular outflow tract obstruction
- overriding aorta (aorta arises from RV instead of LV)
- 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
transposition of great arteries
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
tricuspid atresia
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
pulmonary atresia
failure of pulmonary valve to develop, blind pouch
high ventricular pressure in R side of heart
associated with underdeveloped tricuspid valve
truncus arteriosus
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
hypoplastic left heart syndrome (HLHS)
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
CHD management
Identify and refer immediately to pedi cardiology
correct underlying problem
oxygen - caution in L to R shunt (acyanotic)
two consequences: HF or death
management of “tet” spells
knee-chest position oxygen therapy IV fluid bolus morphine IV BB IV pheynylephrine
Afib causes/RF
idiopathic HTN valvular heart dx hypothyroidism CAD cardiomyopathies HF OSA obesity alcohol drugs
afib presentation
asymptomatic
fatigue, palpitations, weakness, dizziness, reduced exercise tolerance
afib diagnostics
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
afib management
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
CHADS VAS score
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)
CHADS VAS score risk
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
cardioversion
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
urgent cardioversion anticoags
heparin, then warfarin for 4 weeks
non-urgent cardioversion anticoags
start warfarin 3 weeks prior and continue for 4 weeks
young pts and afib
attempt to restore to NSR to prevent remodeling and symptoms at night
PCP role in afib
ID afib, determine risk of stroke, initiate anticoags
Get an ECHO!
Consider antiarrhythmic meds
Paroxysmal afib
Occurs for < 7 days & self terminates
Persistent afib
> 7 days or resolved w/ cardioversion after 48 hrs
Permanent afib
No further efforts are being pursued to restore NSR
atrial flutter
Sawtooth pattern!! 4 flutters to 1 QRS conduction
Results from an abnormality of conduction in the atrium
Ventricles working normally
Supraventricular Tachycardia (SVT)
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!!!
Q waves on EKG
pathologic
suggestive of prior myocardial injury
pacemaker needed in
second degree AV block type 2
third degree AV block
1st degree AV block
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
2nd degree AV block type 1
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)
2nd degree AV block type 2
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
causes of 2nd degree AV block type 2
anterior MI septal infarct fibrosis autoimmune - lupus myocarditis lyme dx meds electrolyte imbalances
3rd degree AV block
complete absence of AV node conduction
P waves NEVER r/t QRS, disassociation between them
HIGH RISK asystole, Vtach, DEATH
NEEDS PACEMAKER
3rd degree AV block causes
post MI
meds: BB, CCB, adenosine, amiodarone
Wolf Parkinson white Syndrome
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
v tach
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
antiarrythmic agents
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
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
C. mitral regurgitation
heard at apex (mitral point), systolic murmur
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.
D. 15 y.o.
heart is growing and stretching
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?
Yes, significant is the chest pain angina?
murmur is most likely aortic stenosis
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
C. diastolic sounds heard loudest near apex
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
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.
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
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
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. 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
The valve most commonly involved in chronic rheumatic heart dx
A. aortic
B. mitral
C. pulmonic
D. tricuspid
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.
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 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.
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. 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.
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
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.
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
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.
The diagnosis of mitral valve prolapse can be confirmed by:
A. CXR
B. Echo
C. EKG
D. physical exam
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.
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
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.
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
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.
